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        <title>Cellular and Molecular Immunology via MedWorm.com</title>
        <description>MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest items from the 'Cellular and Molecular Immunology' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Cellular+and+Molecular+Immunology&t=Cellular+and+Molecular+Immunology&s=Search&f=source]]></link>
        <lastBuildDate>Thu, 09 Feb 2012 16:56:39 +0100</lastBuildDate>
        <item>
            <title>C-type lectin receptor-induced NF-κB activation in innate immune and inflammatory responses.</title>
            <link>http://www.medworm.com/index.php?rid=5598794&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22246129%26dopt%3DAbstract</link>
            <description>Authors: Kingeter LM, Lin X
    Abstract
    The C-type lectin receptors (CLRs) belong to a large family of proteins that contain a carbohydrate recognition domain (CRD) and calcium binding sites on their extracellular domains. Recent studies indicate that many CLRs, such as Dectin-1, Dectin-2 and Mincle, function as pattern recognition receptors (PRRs) recognizing carbohydrate ligands from infected microorganisms. Upon ligand binding, these CLRs induce multiple signal transduction cascades through their own immunoreceptor tyrosine-based activation motifs (ITAMs) or interacting with ITAM-containing adaptor proteins such as FcRγ. Emerging evidence indicate that CLR-induced signaling cascades lead to the activation of nuclear factor kappaB (NF-κB) family of transcriptional factors through ...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5598794</comments>
            <pubDate>Mon, 16 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5598794</guid>        </item>
        <item>
            <title>Improved survival ratios correlate with myeloid dendritic cell restoration in acute-on-chronic liver failure patients receiving methylprednisolone therapy.</title>
            <link>http://www.medworm.com/index.php?rid=5598798&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22231552%26dopt%3DAbstract</link>
            <description>Authors: Zhao J, Zhang JY, Yu HW, He YL, Zhao JJ, Li J, Zhu YK, Yao QW, Wang JH, Liu HX, Shi SY, Zou ZS, Xu XS, Zhou CB, Wang FS, Meng QH
    Abstract
    Acute-on-chronic liver failure (ACLF) is a severe life-threatening complication. Liver transplantation is the only available therapeutic option; however, several limitations have restricted its use in patients. The use of corticosteroids as an optional therapy for ACLF has received a great deal of interest. The rationale behind its use is the possible role of the immune system in initiating and perpetuating hepatic damage. In order to assess the relationship between myeloid dendritic cells (mDCs) and the efficacy of methylprednisolone (MP) treatment for hepatitis B virus (HBV)-associated ACLF patients, we recruited 30 HBV-associated ACLF...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5598798</comments>
            <pubDate>Mon, 09 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5598798</guid>        </item>
        <item>
            <title>Immune receptor signaling: from ubiquitination to NF-κB activation.</title>
            <link>http://www.medworm.com/index.php?rid=5598797&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22231553%26dopt%3DAbstract</link>
            <description>Authors: Sun SC
    PMID: 22231553 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5598797</comments>
            <pubDate>Mon, 09 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5598797</guid>        </item>
        <item>
            <title>Salmeterol attenuates the inflammatory response in asthma and decreases the pro-inflammatory cytokine secretion of dendritic cells.</title>
            <link>http://www.medworm.com/index.php?rid=5598796&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22231554%26dopt%3DAbstract</link>
            <description>In conclusion, we provide evidence that DCs are the target immune cells responsible for the action of salmeterol against asthma.Cellular &amp; Molecular Immunology advance online publication, 9 January 2012; doi:10.1038/cmi.2011.56.
    PMID: 22231554 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5598796</comments>
            <pubDate>Mon, 09 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5598796</guid>        </item>
        <item>
            <title>Identification of novel HLA-A*0201-restricted epitopes from anterior gradient-2 as a tumor-associated antigen against colorectal cancer.</title>
            <link>http://www.medworm.com/index.php?rid=5598795&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22231555%26dopt%3DAbstract</link>
            <description>In conclusion, these novel epitopes derived from AGR2 protein may be attractive candidates for DC-based immunotherapy for CRC.Cellular &amp; Molecular Immunology advance online publication, 9 January 2012; doi:10.1038/cmi.2011.52.
    PMID: 22231555 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5598795</comments>
            <pubDate>Mon, 09 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5598795</guid>        </item>
        <item>
            <title>Identification of HBsAg-specific antibodies from a mammalian cell displayed full-length human antibody library of healthy immunized donor.</title>
            <link>http://www.medworm.com/index.php?rid=5533251&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22179672%26dopt%3DAbstract</link>
            <description>Authors: Li CZ, Liang ZK, Chen ZR, Lou HB, Zhou Y, Zhang ZH, Yu F, Liu S, Zhou Y, Wu S, Zheng W, Tan W, Jiang S, Zhou C
    Abstract
    Hepatitis B immunoglobulin (HBIG) is important in the management of hepatitis B virus (HBV) infection. Aiming to develop recombinant monoclonal antibodies as an alternative to HBIG, we report the successful identification of HBV surface antigen (HBsAg)-specific antibodies from a full-length human antibody library displayed on mammalian cell surface. Using total RNA of peripheral blood mononuclear cells of a natively immunized donor as template, the antibody repertoire was amplified. Combining four-way ligation and the Flp recombinase-mediated integration (Flp-In) system, we constructed a mammalian cell-based, fully human, full-length antibody display libr...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5533251</comments>
            <pubDate>Mon, 19 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5533251</guid>        </item>
        <item>
            <title>IL-17 initiates tertiary lymphoid organ formation.</title>
            <link>http://www.medworm.com/index.php?rid=5533250&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22179673%26dopt%3DAbstract</link>
            <description>Authors: Zhang X, Lu B
    PMID: 22179673 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5533250</comments>
            <pubDate>Mon, 19 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5533250</guid>        </item>
        <item>
            <title>Liver fibrosis: mechanisms of immune-mediated liver injury.</title>
            <link>http://www.medworm.com/index.php?rid=5533253&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22157623%26dopt%3DAbstract</link>
            <description>Authors: Xu R, Zhang Z, Wang FS
    Abstract
    Liver fibrosis and its end-stage consequence, cirrhosis, represent the final common pathway of virtually all chronic liver diseases. Research into hepatic stellate cell activation, imbalance of the extracellular matrix synthesis and degradation and the contribution of cytokines and chemokines has further elucidated the mechanisms underlying fibrosis. Furthermore, clarification of changes in host adaptive and innate immune systems has accelerated our understanding of the association between liver inflammation and fibrosis. Continued elucidation of the mechanisms of hepatic fibrosis has provided a comprehensive model of fibrosis progression and regression. This review summarizes the current concepts of improvements that have been made in the f...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5533253</comments>
            <pubDate>Mon, 12 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5533253</guid>        </item>
        <item>
            <title>New immune therapy targets tumor-associated environment: from bone marrow to tumor site.</title>
            <link>http://www.medworm.com/index.php?rid=5533252&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22157624%26dopt%3DAbstract</link>
            <description>Authors: Fu YX
    PMID: 22157624 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5533252</comments>
            <pubDate>Mon, 12 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5533252</guid>        </item>
        <item>
            <title>Antigen-presenting effects of effector memory Vγ9Vδ2 T cells in rheumatoid arthritis.</title>
            <link>http://www.medworm.com/index.php?rid=5533254&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22139198%26dopt%3DAbstract</link>
            <description>This study investigated the antigen-presenting effects of γδ T cells and their relationship with rheumatoid arthritis development. We found that Vγ9Vδ2 T cells (the predominant subtype of γδ T cells in peripheral blood) were activated by isopentenyl pyrophosphate to continuously proliferate and differentiate into effector memory cells. The effector memory Vγ9Vδ2 T cells exhibited phenotypic characteristics of specific antigen-presenting cells, including high HLA-DR and CD80/86 expression. These Vγ9Vδ2 T cells could present soluble antigens and synthetic peptides to CD4(+) T cells. Vγ9Vδ2 T cells with different phenotypes showed different cytokine secretion patterns. Effector memory Vγ9Vδ2 T cells simultaneously secreted not only interferon (IFN)-γ but also IL-17. The periphe...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5533254</comments>
            <pubDate>Mon, 05 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5533254</guid>        </item>
        <item>
            <title>Targeting and utilizing primary tumors as live vaccines: changing strategies.</title>
            <link>http://www.medworm.com/index.php?rid=5439655&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22101245%26dopt%3DAbstract</link>
            <description>Authors: Yang X, Mortenson ED, Fu YX
    Abstract
    Tumor metastases and relapse are the major causes of morbidity and mortality in cancer. Although surgery, chemotherapy and/or radiation therapy can typically control primary tumor growth, metastatic and relapsing tumors are often inaccessible or resistant to these treatments. An adaptive immune response can be generated during these conventional treatments of the primary tumor, and presumably both the primary tumor and secondary metastases share many of the same or similar antigenic characteristics recognized by the immune system. Thus, when established, this response should be able to control metastatic growth and tumor relapse. This review summarizes the mechanisms by which antitumor immune responses are generated, and recent findings...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5439655</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5439655</guid>        </item>
        <item>
            <title>Promotion of cell proliferation and inhibition of ADCC by cancerous immunoglobulin expressed in cancer cell lines.</title>
            <link>http://www.medworm.com/index.php?rid=5379320&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22036905%26dopt%3DAbstract</link>
            <description>Authors: Li M, Zheng H, Duan Z, Liu H, Hu D, Bode A, Dong Z, Cao Y
    Abstract
    To explore the significance of cancerous immunoglobulin (Ig) in cancer cell growth, HeLa cervical cancer cells were stably transfected with small interfering RNA (siRNA) that specifically, efficiently and consistently silences the expression of heavy chain genes of all immunoglobulin isotypes. This stable cell line was used to examine cell viability, colony formation and tumor growth in athymic nude mice. The results of these experiments indicated that siRNA-mediated knockdown of cancerous Ig inhibited cell growth in vitro and suppressed tumor cell growth in immune-deficient nude mice in vivo. Similarly, this siRNA also inhibited the growth of MGC gastric cancer cells and MCF-7 breast cancer cells. Furtherm...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379320</comments>
            <pubDate>Mon, 31 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379320</guid>        </item>
        <item>
            <title>Bone marrow and the control of immunity.</title>
            <link>http://www.medworm.com/index.php?rid=5379321&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22020068%26dopt%3DAbstract</link>
            <description>Authors: Zhao E, Xu H, Wang L, Kryczek I, Wu K, Hu Y, Wang G, Zou W
    Abstract
    Bone marrow is thought to be a primary hematopoietic organ. However, accumulated evidences demonstrate that active function and trafficking of immune cells, including regulatory T cells, conventional T cells, B cells, dendritic cells, natural killer T (NKT) cells, neutrophils, myeloid-derived suppressor cells and mesenchymal stem cells, are observed in the bone marrow. Furthermore, bone marrow is a predetermined metastatic location for multiple human tumors. In this review, we discuss the immune network in the bone marrow. We suggest that bone marrow is an immune regulatory organ capable of fine tuning immunity and may be a potential therapeutic target for immunotherapy and immune vaccination.Cellular &amp;amp...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379321</comments>
            <pubDate>Mon, 24 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379321</guid>        </item>
        <item>
            <title>Direct regulation of interleukin-6 expression by Notch signaling in macrophages.</title>
            <link>http://www.medworm.com/index.php?rid=5312063&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21983868%26dopt%3DAbstract</link>
            <description>In this study, we investigated the role of Notch signaling in the regulation of the IL-6 transcript in murine macrophages. The upregulation of Notch1 protein levels and the appearance of cleaved Notch1 (Val1744) correlated well with the increased IL-6 mRNA expression levels in murine primary bone marrow-derived macrophages (BMMφ) after activation by lipopolysaccharide (LPS) together with interferon-gamma (IFN-γ). Treatment of BMMφ with the γ-secretase inhibitor IL-CHO to suppress the transduction of Notch signaling resulted in a partial decrease in the level of IL-6 mRNA and the amount of IL-6 protein produced. In contrast, the overexpression of a constitutively activated intracellular Notch1 protein (N(IC)) in the RAW264.7 macrophage-like cell line resulted in significantly higher IL-...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5312063</comments>
            <pubDate>Mon, 10 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5312063</guid>        </item>
        <item>
            <title>Impairment of non-muscle myosin IIA in human CD4(+) T cells contributes to functional deficits in the elderly.</title>
            <link>http://www.medworm.com/index.php?rid=5312062&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21983869%26dopt%3DAbstract</link>
            <description>In this study, we describe a series of experiments supporting the hypothesis that effective TCR downmodulation requires not only efficient reorganization of the actin cytoskeleton, but also functional NMMIIA. For the first time, we show that CD4(+) T cells from elderly human donors have dysfunctional NMMIIA that contributes to delaying activation-induced TCR internalization and impairing calcium mobilization. Additionally, our results demonstrate that chemical inhibition of NMMIIA in CD4(+) T cells from young donors also results in complete abrogation of TCR internalization, strongly supporting the fundamental role of NMMIIA in modulating this event. Recent observations that the generation of an efficient T-cell response requires migration prompted us to investigate whether NMMIIA also pla...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5312062</comments>
            <pubDate>Mon, 10 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5312062</guid>        </item>
        <item>
            <title>Alterations of peripheral CD4(+)CD25(+)Foxp3(+) T regulatory cells in mice with STZ-induced diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=5312061&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21983870%26dopt%3DAbstract</link>
            <description>Authors: Zhen Y, Sun L, Liu H, Duan K, Zeng C, Zhang L, Jin D, Peng J, Ding W, Zhao Y
    Abstract
    Complications arising from abnormal immune responses are the major causes of mortality and morbidity in diabetic patients. CD4(+)CD25(+) T regulatory cells (Tregs) play pivotal roles in controlling immune homeostasis, immunity and tolerance. The effect of hyperglycemia on CD4(+)CD25(+) Tregs has not yet been addressed. Here we used streptozotocin (STZ)-induced diabetic mice to study the effects of long-term hyperglycemia on CD4(+)CD25(+) Tregs in vivo. Four months after the onset of diabetes, the frequency of CD4(+)CD25(+)Foxp3(+) T regulatory cells was significantly elevated in the spleen, peripheral blood lymphocytes (PBLs), peripheral lymph nodes (pLNs) and mesenteric LNs (mLNs). CD4(+...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5312061</comments>
            <pubDate>Mon, 10 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5312061</guid>        </item>
        <item>
            <title>The efficacy of miRNA122, a novel therapeutic target, for predicting the progression of hepatocellular carcinoma (HCC).</title>
            <link>http://www.medworm.com/index.php?rid=5312060&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21983871%26dopt%3DAbstract</link>
            <description>Authors: Wang L, Zhang Z, Wang FS
    PMID: 21983871 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5312060</comments>
            <pubDate>Mon, 10 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5312060</guid>        </item>
        <item>
            <title>Activation of human fibroblast-like synoviocytes by uric acid crystals in rheumatoid arthritis.</title>
            <link>http://www.medworm.com/index.php?rid=5277108&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21946433%26dopt%3DAbstract</link>
            <description>Authors: Chen DP, Wong CK, Tam LS, Li EK, Lam CW
    Abstract
    Hyperuricemia-mediated uric acid crystal formation may cause joint inflammation and provoke the destruction of joints through the activation of inflammasome-mediated innate immune responses. However, the immunopathological effects and underlying intracellular regulatory mechanisms of uric acid crystal-mediated activation of fibroblast-like synoviocytes (FLS) in rheumatoid arthritis (RA) have not been elucidated. Therefore, we investigated the in vitro effects of monosodium urate crystals, alone or in combination with the inflammatory cytokines tumor-necrosis factor (TNF)-α or interleukin (IL)-1β, on the activation of human FLS from RA patients and normal control subjects and the underlying intracellular signaling mechanism...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5277108</comments>
            <pubDate>Mon, 26 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5277108</guid>        </item>
        <item>
            <title>A critical role of IL-17 in modulating the B-cell response during H5N1 influenza virus infection.</title>
            <link>http://www.medworm.com/index.php?rid=5277107&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21946434%26dopt%3DAbstract</link>
            <description>In this study, we show that H5N1-infected IL-17 knockout (KO) mice exhibit markedly increased weight loss, more pronounced lung immunopathology and significantly reduced survival rates as compared with infected wild-type controls. Moreover, the frequency of B cells in the lung were substantially decreased in IL-17 KO mice after virus infection, which correlated with reduced CXCR5 expression in B cells and decreased CXCL13 production in the lung tissue of IL-17 KO mice. Consistent with this observation, B cells from IL-17 KO mice exhibited a significant reduction in chemokine-mediated migration in culture. Taken together, these findings demonstrate a critical role for IL-17 in mediating the recruitment of B cells to the site of pulmonary influenza virus infection in mice.Cellular &amp; Mole...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5277107</comments>
            <pubDate>Mon, 26 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5277107</guid>        </item>
        <item>
            <title>Regulation of antiviral innate immunity by deubiquitinase CYLD.</title>
            <link>http://www.medworm.com/index.php?rid=5277106&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21946435%26dopt%3DAbstract</link>
            <description>Authors: Zhang M, Lee AJ, Wu X, Sun SC
    Abstract
    An antiviral innate immune response involves induction of type I interferons (IFNs) and their subsequent autocrine and paracrine actions, but the underlying regulatory mechanisms are incompletely understood. Here we report that CYLD, a deubiquitinase that specifically digests lysine 63-linked ubiquitin chains, is required for antiviral host defense. Loss of CYLD renders mice considerably more susceptible to infection by vesicular stomatitis virus (VSV). Consistently, CYLD-deficient dendritic cells are more sensitive to VSV infection. This functional defect was not due to lack of type I IFN production but rather because of attenuated IFN receptor signaling. In the absence of CYLD, IFN-β is ineffective in the induction of antiviral gen...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5277106</comments>
            <pubDate>Mon, 26 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5277106</guid>        </item>
        <item>
            <title>Proinflammatory IL-17 induces iBALT development.</title>
            <link>http://www.medworm.com/index.php?rid=5246168&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21927015%26dopt%3DAbstract</link>
            <description>Authors: Zhu M, Fu Y
    PMID: 21927015 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5246168</comments>
            <pubDate>Mon, 19 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5246168</guid>        </item>
        <item>
            <title>SHP gains citizenship of the AMPK kingdom.</title>
            <link>http://www.medworm.com/index.php?rid=5246167&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21927016%26dopt%3DAbstract</link>
            <description>Authors: Chung HT
    PMID: 21927016 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5246167</comments>
            <pubDate>Mon, 19 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5246167</guid>        </item>
        <item>
            <title>Endocytosis by target cells: an essential means for perforin- and granzyme-mediated killing.</title>
            <link>http://www.medworm.com/index.php?rid=5246166&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21927017%26dopt%3DAbstract</link>
            <description>Authors: Gordy C, He YW
    PMID: 21927017 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5246166</comments>
            <pubDate>Mon, 19 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5246166</guid>        </item>
        <item>
            <title>IL-17, a new kid on the block of tertiary lymphoid organs.</title>
            <link>http://www.medworm.com/index.php?rid=5246165&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21927018%26dopt%3DAbstract</link>
            <description>Authors: Lu TT, Kim H, Ma X
    PMID: 21927018 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5246165</comments>
            <pubDate>Mon, 19 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5246165</guid>        </item>
        <item>
            <title>IKKi: a novel regulator of Act1, IL-17 signaling and pulmonary inflammation.</title>
            <link>http://www.medworm.com/index.php?rid=5246164&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21927019%26dopt%3DAbstract</link>
            <description>Authors: Shembade N, Harhaj EW
    PMID: 21927019 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5246164</comments>
            <pubDate>Mon, 19 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5246164</guid>        </item>
        <item>
            <title>Discrimination of membrane antigen affinity by B cells requires dominance of kinetic proofreading over serial engagement.</title>
            <link>http://www.medworm.com/index.php?rid=5218498&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21909127%26dopt%3DAbstract</link>
            <description>Authors: Tsourkas PK, Liu W, Das SC, Pierce SK, Raychaudhuri S
    Abstract
    B-cell receptor signaling in response to membrane-bound antigen increases with antigen affinity, a process known as affinity discrimination. We use computational modeling to show that B-cell affinity discrimination requires that kinetic proofreading predominate over serial engagement. We find that if B-cell receptors become signaling-capable immediately upon antigen binding, which results in decreasing serial engagement as affinity increases, then increasing affinity can lead to weaker signaling. Rather, antigen must stay bound to B-cell receptors for a threshold time of several seconds before becoming signaling-capable, a process similar to kinetic proofreading. This process overcomes the loss in serial engage...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5218498</comments>
            <pubDate>Mon, 12 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5218498</guid>        </item>
        <item>
            <title>CDR3δ -grafted γ9δ2T cells mediate effective antitumor reactivity.</title>
            <link>http://www.medworm.com/index.php?rid=5218497&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21909128%26dopt%3DAbstract</link>
            <description>Authors: Zhao H, Xi X, Cui L, He W
    Abstract
    Adoptive cell-transfer therapy (ACT) has been reported to suppress growing tumors and to overcome tumor escape in animal models. As a candidate ACT effector, γ9δ2T cells can be activated and expanded in vitro and in vivo and display strong antitumor activity against colorectal, lung, prostate, ovarian and renal cell carcinomas. However, it is difficult to obtain a large enough number of γδT cells to meet the need for immunotherapy that can overcome the cancer patients' immune suppressive tumor microenvironment. In previous studies, our lab confirmed that γ9δ2T cells recognized tumor cells via the CDR3δ region of the γδ-T-cell receptor (TCR). We constructed full-length human peripheral blood mononuclear cell (PBMC)-derived γ9 and...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5218497</comments>
            <pubDate>Mon, 12 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5218497</guid>        </item>
        <item>
            <title>Neutrophils, reverse traffic and detrimental potential.</title>
            <link>http://www.medworm.com/index.php?rid=5192546&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21874043%26dopt%3DAbstract</link>
            <description>Authors: Zeng G, Chen ZW
    PMID: 21874043 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5192546</comments>
            <pubDate>Sun, 28 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5192546</guid>        </item>
        <item>
            <title>Heterogeneity of aberrant immunoglobulin expression in cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=5157021&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21860405%26dopt%3DAbstract</link>
            <description>Authors: Hu D, Duan Z, Li M, Jiang Y, Liu H, Zheng H, Li L, Bode AM, Dong Z, Cao Y
    Abstract
    Accumulating evidence has shown that immunoglobulin (Ig) is 'unexpectedly' expressed by epithelial cancer cells and that it can promote tumor growth. The main purpose of this study was to explore the components of the cancerous Ig and its possible function. The presence of cancerous Ig in the Golgi apparatus was confirmed by immunofluorescence, indirectly suggesting that the cancerous Ig was processed and packaged in cancer cells. Western blot analysis and ELISA results indicated that cancer cells produced membrane Ig and secreted Ig into the supernatant fraction. The cancerous Ig consists of an α heavy chain and a κ light chain. Finally, by analyzing the Ig components pulled down by prote...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5157021</comments>
            <pubDate>Sun, 21 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5157021</guid>        </item>
        <item>
            <title>Novel insights into the molecular mechanisms of α-fetoprotein expression and malignant phenotypes of hepatocellular carcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=5157020&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21860406%26dopt%3DAbstract</link>
            <description>Authors: Hu Z, Zhao W
    PMID: 21860406 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5157020</comments>
            <pubDate>Sun, 21 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5157020</guid>        </item>
        <item>
            <title>MicroRNA immunobiology: when microRNA chemists meet immunologists.</title>
            <link>http://www.medworm.com/index.php?rid=5157019&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21860407%26dopt%3DAbstract</link>
            <description>Authors: Chen YH
    PMID: 21860407 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5157019</comments>
            <pubDate>Sun, 21 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5157019</guid>        </item>
        <item>
            <title>SHP limits TLR signaling, an inducible transcriptional corepressor.</title>
            <link>http://www.medworm.com/index.php?rid=5157018&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21860408%26dopt%3DAbstract</link>
            <description>Authors: Zhang J, Shen B
    PMID: 21860408 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5157018</comments>
            <pubDate>Sun, 21 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5157018</guid>        </item>
        <item>
            <title>Chimeric flagellin expressed by Salmonella typhimurium induces an ESAT-6-specific Th1-type immune response and CTL effects following intranasal immunization.</title>
            <link>http://www.medworm.com/index.php?rid=5141226&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21841816%26dopt%3DAbstract</link>
            <description>Authors: Zhang H, Liu L, Wen K, Huang J, Geng S, Shen J, Pan Z, Jiao X
    Abstract
    The flagellin component FliC of Salmonella typhimurium is capable of activating the innate immune system via specific interactions with TLR5 and can also act as a carrier of foreign antigen to elicit antigen-specific immune responses. Thus, we constructed an attenuated Salmonella strain SL5928(fliC/esat) expressing chimeric flagellin that contained the ESAT-6 antigen coding sequence of Mycobacterium tuberculosis inserted into the highly variable region of the Salmonella flagellin coding gene fliC(i). The chimeric flagellin functioned normally, as demonstrated using a flagella swarming assay and electron microscopy. To analyze the effects of chimeric flagellin, the cell-mediated immune response and cytot...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141226</comments>
            <pubDate>Sun, 14 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141226</guid>        </item>
        <item>
            <title>MicroRNA in TLR signaling and endotoxin tolerance.</title>
            <link>http://www.medworm.com/index.php?rid=5141229&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21822296%26dopt%3DAbstract</link>
            <description>Authors: Nahid MA, Satoh M, Chan EK
    Abstract
    Toll-like receptors (TLRs) in innate immune cells are the prime cellular sensors for microbial components. TLR activation leads to the production of proinflammatory mediators and thus TLR signaling must be properly regulated by various mechanisms to maintain homeostasis. TLR4-ligand lipopolysaccharide (LPS)-induced tolerance or cross-tolerance is one such mechanism, and it plays an important role in innate immunity. Tolerance is established and sustained by the activity of the microRNA miR-146a, which is known to target key elements of the myeloid differentiation factor 88 (MyD88) signaling pathway, including IL-1 receptor-associated kinase (IRAK1), IRAK2 and tumor-necrosis factor (TNF) receptor-associated factor 6 (TRAF6). In this revie...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141229</comments>
            <pubDate>Sun, 07 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141229</guid>        </item>
        <item>
            <title>Optimal culture conditions for the generation of natural killer cell-induced dendritic cells for cancer immunotherapy.</title>
            <link>http://www.medworm.com/index.php?rid=5141228&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21822297%26dopt%3DAbstract</link>
            <description>Authors: Nguyen-Pham TN, Yang DH, Nguyen TA, Lim MS, Hong CY, Kim MH, Lee HJ, Lee YK, Cho D, Bae SY, Ahn JS, Kim YK, Chung IJ, Kim HJ, Lee JJ
    Abstract
    Dendritic cell (DC)-based vaccines continue to be considered an attractive tool for cancer immunotherapy. DCs require an additional signal from the environment or other immune cells to polarize the development of immune responses toward T helper 1 (Th1) or Th2 responses. DCs play a role in natural killer (NK) cell activation, and NK cells are also able to activate and induce the maturation of DCs. We investigated the types of NK cells that can induce the maturation and enhanced function of DCs and the conditions under which these interactions occur. DCs that were activated by resting NK cells in the presence of inflammatory cytokines...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141228</comments>
            <pubDate>Sun, 07 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141228</guid>        </item>
        <item>
            <title>MicroRNAs are key regulators controlling iNKT and regulatory T-cell development and function.</title>
            <link>http://www.medworm.com/index.php?rid=5141227&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21822298%26dopt%3DAbstract</link>
            <description>Authors: Zhou L, Park JJ, Zheng Q, Dong Z, Mi Q
    Abstract
    MicroRNAs (miRNAs) are an abundant class of evolutionarily conserved, small, non-coding RNAs that post-transcriptionally regulate expression of their target genes. Emerging evidence indicates that miRNAs are important regulators that control the development, differentiation and function of different immune cells. Both CD4(+)CD25(+)Foxp3(+) regulatory T (Treg) cells and invariant natural killer T (iNKT) cells are critical for immune homeostasis and play a pivotal role in the maintenance of self-tolerance and immunity. Here, we review the important roles of miRNAs in the development and function of iNKT and Treg cells.Cellular &amp; Molecular Immunology advance online publication, 8 August 2011; doi:10.1038/cmi.2011.27.
    PMI...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141227</comments>
            <pubDate>Sun, 07 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141227</guid>        </item>
        <item>
            <title>The altered expression of inflammation-related microRNAs with microRNA-155 expression correlates with Th17 differentiation in patients with acute coronary syndrome.</title>
            <link>http://www.medworm.com/index.php?rid=5097616&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21804579%26dopt%3DAbstract</link>
            <description>In conclusion, our study revealed the expression patterns of inflammation-related miRNAs in patients with ACS and found that miR-155 may be associated with Th17 cell differentiation.Cellular &amp; Molecular Immunology advance online publication, 1 August 2011; doi:10.1038/cmi.2011.22.
    PMID: 21804579 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5097616</comments>
            <pubDate>Sun, 31 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5097616</guid>        </item>
        <item>
            <title>Efficient induction of a Her2-specific anti-tumor response by dendritic cells pulsed with a Hsp70L1-Her2(341-456) fusion protein.</title>
            <link>http://www.medworm.com/index.php?rid=5097631&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21785448%26dopt%3DAbstract</link>
            <description>Authors: Fu Q, Wu Y, Yan F, Wang N, Wang W, Cao X, Wang Y, Wan T
    Heat shock proteins (HSPs) have been shown to interact with antigen-presenting cells (APCs), especially dendritic cells (DCs). HSPs act as potent adjuvants, inducing a Th1 response, as well as antigen-specific CD8(+) cytotoxic T lymphocytes (CTL) via cross-presentation. Our previous work has demonstrated that Hsp70-like protein 1 (Hsp70L1), a new member of the Hsp70 subfamily, can act as a powerful Th1 adjuvant in a DC-based vaccine. Here we report the efficient induction of tumor antigen-specific T cell immune response by DCs pulsed with recombinant fusion protein of Hsp70L1 and Her2(341-456), the latter of which is a fragment of Her2/neu (Her2) containing E75 (a HLA-A2 restricted CTL epitope). The fusion protein Hsp70L1...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5097631</comments>
            <pubDate>Sun, 24 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5097631</guid>        </item>
        <item>
            <title>MicroRNA regulation of innate immune responses in epithelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=5000977&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21725335%26dopt%3DAbstract</link>
            <description>Authors: Zhou R, O'Hara SP, Chen XM
    Mucosal surface epithelial cells are equipped with several defense mechanisms that guard against pathogens. Recent studies indicate that microRNAs (miRNAs) mediate post-transcriptional gene suppression and may be a critical component of the complex regulatory networks in epithelial immune responses. Transcription of miRNA genes in epithelial cells can be elaborately controlled through pathogen recognition receptors, such as Toll-like receptors (TLRs), and associated nuclear factor kappaB (NF-κB) and mitogen-activated protein kinase (MAPK) pathways, and ultimately nuclear transcription factor associated-transactivation and transrepression. Activation of these intracellular signaling pathways may also modulate the process of miRNA maturation. Function...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5000977</comments>
            <pubDate>Sun, 03 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5000977</guid>        </item>
        <item>
            <title>EBV-induced human CD8(+) NKT cells synergize CD4(+) NKT cells suppressing EBV-associated tumors upon induction of Th1 bias.</title>
            <link>http://www.medworm.com/index.php?rid=5000978&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21725328%26dopt%3DAbstract</link>
            <description>Authors: Xiao W, Li L, Zhou R, Xiao R, Wang Y, Ji X, Wu M, Wang L, Huang W, Zheng X, Tan X, Chen L, Xiong T, Xiong J, Jin Y, Tan J, He Y
    
    PMID: 21725328 [PubMed - in process] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5000978</comments>
            <pubDate>Thu, 30 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5000978</guid>        </item>
        <item>
            <title>HMBOX1 negatively regulates NK cell functions by suppressing the NKG2D/DAP10 signaling pathway.</title>
            <link>http://www.medworm.com/index.php?rid=5000979&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21706044%26dopt%3DAbstract</link>
            <description>Authors: Wu L, Zhang C, Zhang J
    HMBOX1 is a new member of the homeobox family. Homeobox members have been reported to participate in embryonic development and systemic metabolism, but the function of HMBOX1 remains unclear, especially in the hematopoietic system. Here, we show that HMBOX1 is expressed at a high level in primary human NK cells but is expressed at much lower levels in NK cell lines. Overexpression of HMBOX1 significantly inhibited NK cell activities, including natural cytotoxicity against tumor cells, the level of CD107a (a marker protein for degranulation) and the production of cytolytic proteins (perforin and granzymes). More interestingly, HMBOX1 negatively regulated the expression of NKG2D and the activation of the NKG2D/DAP10 signaling pathway in NK cells. This effe...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5000979</comments>
            <pubDate>Sun, 26 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5000979</guid>        </item>
        <item>
            <title>Strategies of mucosal immunotherapy for allergic diseases.</title>
            <link>http://www.medworm.com/index.php?rid=4956127&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21666705%26dopt%3DAbstract</link>
            <description>This study reviews recent progress in mucosal immunotherapy for allergic diseases. Administration routes, antigen quality and quantity, and adjuvants used are major considerations in this field. Also, direct uses of unique probiotics, or specific cytokines, have been discussed. Furthermore, some researchers have reported new therapeutic ideas that combine two or more strategies. The most important strategy for development of mucosal therapies for allergic diseases is the improvement of antigen formulation, which includes continuous searching for efficient adjuvants, collecting more information about dominant T-cell epitopes of allergens, and having the proper combination of each. In clinics, when compared to other mucosal routes, sublingual immunotherapy (SLIT) is a preferred choice for th...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4956127</comments>
            <pubDate>Sun, 12 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4956127</guid>        </item>
        <item>
            <title>Anti-γδ TCR antibody-expanded γδ T cells: a better choice for the adoptive immunotherapy of lymphoid malignancies.</title>
            <link>http://www.medworm.com/index.php?rid=4956126&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21666706%26dopt%3DAbstract</link>
            <description>In this study, we found that adoptive transfer of the expanded γδ T cells to Daudi lymphoma-bearing nude mice significantly prolonged the survival time of the mice and improved their living status. We further investigated the characteristics of these antibody-expanded γδ T cells compared to the more commonly used phosphoantigen-expanded γδ T cells and evaluated the feasibility of employing them in the treatment of lymphoid malignancies. Slow but sustained proliferation of human peripheral blood γδ T cells was observed upon stimulation with anti-γδ TCR antibody. Compared to phosphoantigen-stimulated γδ T cells, the antibody-expanded cells manifested similar functional phenotypes and cytotoxic activity towards lymphoma cell lines. It is noteworthy that the anti-γδ TCR antibody ...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4956126</comments>
            <pubDate>Sun, 12 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4956126</guid>        </item>
        <item>
            <title>Persistence of tumor-infiltrating CD8 T cells is tumor-dependent but antigen-independent.</title>
            <link>http://www.medworm.com/index.php?rid=4956125&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21666707%26dopt%3DAbstract</link>
            <description>In this study, we show that tolerant 2C T cells persist in the prostate tumor of TRP-SIY mice by proliferating slowly in a tumor-dependent, but antigen-, interleukin (IL)-7- and IL-15-independent manner. We also show that disappearance of 2C T cells from the lymphoid organs of TRP-SIY mice are due to antigen-induced T-cell contraction rather than altered trafficking or generalized T-cell depletion in the mice. Finally, we show that clonal T cells unreactive to SIY are equally capable of persisting in the prostate tumor. These findings suggest that while functional tolerance of TILs is induced by antigen, persistence of tolerant TILs in the tumor tissue is mediated by a novel mechanism: slow proliferation independent of antigen and homeostatic cytokines. These results also allow CD8 T-cell ...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4956125</comments>
            <pubDate>Sun, 12 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4956125</guid>        </item>
        <item>
            <title>The development and functions of CD4(+) T cells expressing a transgenic TCR specific for an MHC-I-restricted tumor antigenic epitope.</title>
            <link>http://www.medworm.com/index.php?rid=4907032&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21643003%26dopt%3DAbstract</link>
            <description>In this study, we further showed that more than 50% of CD4(+) T cells in MHC-I-restricted P1A tumor antigen-specific TCR (P1ATCR)-transgenic mice could specifically bind to MHC-I/P1A peptide complex. P1A peptide could stimulate the transgenic CD4(+) T cells to proliferate and secrete both type 1 helper T cell and type 2 helper T cell cytokines. The activated CD4(+) T cells also showed cytotoxicity against P1A-expressing tumor cells. The analysis of TCR α-chains showed that these CD4(+) T cells were selected by co-expressing endogenous TCRs. Our results show that CD4(+) T cells from P1ATCR transgenic mice co-expressed an MHC-I-restricted transgenic TCR and another rearranged endogenous TCRs, both of which were functional.Cellular &amp; Molecular Immunology advance online publication, 6 Jun...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4907032</comments>
            <pubDate>Sun, 05 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4907032</guid>        </item>
        <item>
            <title>MLK4 has negative effect on TLR4 signaling.</title>
            <link>http://www.medworm.com/index.php?rid=4856076&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21602844%26dopt%3DAbstract</link>
            <description>Authors: Seit-Nebi A, Cheng W, Xu H, Han J
    The stimulation of Toll-like receptors (TLRs) on macrophages triggers production of proinflammatory cytokines such as tumor-necrosis factor-α (TNF-α). The TNF production is mediated by a series of signaling events and subsequent transcriptional and post-transcriptional activation of the TNF gene. Termination of TLR-mediated cellular signaling is also important for a proper immunoresponse, since sustained cytokine expression can result in immune disorders. Here we identified that mixed-lineage kinase (MLK) 4 is a TLR4-interacting protein. Unlike previously characterized MLK group members, MLK4 cannot act as a mitogen-activated protein kinase kinase kinase (MAP3K) to mediate c-Jun N-terminal kinase (JNK), p38 or extracellular signal-regulated ...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4856076</comments>
            <pubDate>Sun, 22 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4856076</guid>        </item>
        <item>
            <title>Construction of a Der p2-transgenic plant for the alleviation of airway inflammation.</title>
            <link>http://www.medworm.com/index.php?rid=4856075&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21602845%26dopt%3DAbstract</link>
            <description>In this study, we used tobacco plants to develop a large-scale protein production system for allergen-specific immunotherapy, and we investigated the mechanisms of oral tolerance induced by a transgenic plant-derived antigen. We used plants (tobacco leaves) transgenic for the Dermatophagoides pteronyssinus 2 (Der p2) antigen to produce Der p2. Mice received total protein extract from Der p2 orally once per day over 6 days (days 0-2 and days 6-8). Mice were also sensitized and challenged with yeast-derived recombinant Der p2 (rDer p2), after which the mice were examined for airway hyper-responsiveness and airway inflammation. After sensitization and challenge with rDer p2, mice that were fed with total protein extracted from transgenic plants showed decreases in serum Der p2-specific IgE an...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4856075</comments>
            <pubDate>Sun, 22 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4856075</guid>        </item>
        <item>
            <title>Trichosanthin enhances anti-tumor immune response in a murine Lewis lung cancer model by boosting the interaction between TSLC1 and CRTAM.</title>
            <link>http://www.medworm.com/index.php?rid=4856077&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21572449%26dopt%3DAbstract</link>
            <description>In this study, we focused on the effect of TCS on murine anti-tumor immune response in the 3LL Lewis lung carcinoma tumor model and explored the possible molecular pathways involved. In addition to inhibiting cell proliferation and inducing apoptosis in the 3LL tumor, TCS retarded tumor growth and prolonged mouse survival more significantly in C57BL/6 immunocompetent mice than in nude mice. This reflected the fact that the host immune system was involved in tumor eradication. Using FACS analysis, we found that TCS increased the percentage of effector T cells, particularly Interferon-gamma (IFN-γ) producing CD4(+) and CD8(+) T cells from tumor-bearing mice. TCS also promoted the vigorous proliferation of antigen-specific effector T cells, markedly increased Th1 cytokine secretion and elici...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4856077</comments>
            <pubDate>Sun, 15 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4856077</guid>        </item>
        <item>
            <title>An essential role for TAK1 in the contact hypersensitivity response.</title>
            <link>http://www.medworm.com/index.php?rid=4804174&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21552285%26dopt%3DAbstract</link>
            <description>Authors: Zhao YG, Wang Y, Hao W, Wan YY
    Contact hypersensitivity (CHS) is a delayed-type hypersensitivity that can be induced by haptens, such as 2,4-dinitrofluorobenzene (DNFB). Innate and adaptive immunities are both important for the development of CHS. To treat CHS-related diseases, such as allergic contact dermatitis, a disease prevalent in industrialized countries, ways of interfering with improper immune function during CHS responses need to be identified. Transforming growth factor-β-activated kinase-1 (TAK1), a member of mitogen-activated protein kinase kinase kinase family, is important for both innate and adaptive immunities. We thus hypothesized that the CHS response could be inhibited by interfering with TAK1 activity. Using a mouse model in which TAK1 deletion can be loc...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4804174</comments>
            <pubDate>Sun, 08 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4804174</guid>        </item>
        <item>
            <title>Preferential depletion of CD2(low) plasmacytoid dendritic cells in HIV-infected subjects.</title>
            <link>http://www.medworm.com/index.php?rid=4804175&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21516119%26dopt%3DAbstract</link>
            <description>Authors: Du Q, Jiao Y, Hua W, Wang R, Wei F, Ji Y, Du P, Liu YJ, Wu H, Zhang L
    Plasmacytoid dendritic cells (pDCs) are decreased in number and are functionally impaired in HIV act reasons for pDCs depletion are still unknown. It was recently reported that pDCs can be divided into two functionally distinct populations based on their CD2 expression level. To determine how the CD2(high) and CD2(low) populations are affected by HIV infection, we analyzed their frequencies in the peripheral blood of HIV-infected subjects and healthy controls. We found that the CD2(low) pDC subset was preferentially depleted in infected individuals. The frequency of CD2(low) pDCs correlated with the CD4(+) T-cell count but not with the plasma viral load. This finding furthers our understanding of the causes ...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4804175</comments>
            <pubDate>Sun, 24 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4804175</guid>        </item>
        <item>
            <title>The response of intestinal stem cells and epithelium after alemtuzumab administration.</title>
            <link>http://www.medworm.com/index.php?rid=4804176&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21499290%26dopt%3DAbstract</link>
            <description>This study suggests that alemtuzumab treatment induced the increase in stem cells, resulting in the availability of more enterocytes for repair.Cellular &amp; Molecular Immunology advance online publication, 18 April 2011; doi:10.1038/cmi.2011.10.
    PMID: 21499290 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4804176</comments>
            <pubDate>Sun, 17 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4804176</guid>        </item>
        <item>
            <title>The increase in surface CXCR4 expression on lung extravascular neutrophils and its effects on neutrophils during endotoxin-induced lung injury.</title>
            <link>http://www.medworm.com/index.php?rid=4804177&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21460863%26dopt%3DAbstract</link>
            <description>In this study, we found that surface CXCR4 expression increased in extravascular, but not intravascular, neutrophils in the lungs of LPS-induced lung injury model mice. Furthermore, ex vivo studies revealed that CXCL12 acted not only as a chemoattractant, but also as a suppressor of cell death for the lung neutrophils expressing CXCR4. Sulfatide, one of the native ligands for L-selectin, induced the increase of surface CXCR4 expression on isolated circulating neutrophils, suggesting that the activation of L-selectin may be involved in the increase in surface CXCR4. Our findings show that surface CXCR4 levels on neutrophils increase after extravasation into injured lungs, possibly through the activation of L-selectin. The CXCL12/CXCR4 signaling pathway plays an important role in the modulat...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4804177</comments>
            <pubDate>Sun, 03 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4804177</guid>        </item>
        <item>
            <title>Type I and II interferons enhance dendritic cell maturation and migration capacity by regulating CD38 and CD74 that have synergistic effects with TLR agonists.</title>
            <link>http://www.medworm.com/index.php?rid=4638113&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21423200%26dopt%3DAbstract</link>
            <description>Authors: Nguyen-Pham TN, Lim MS, Nguyen TA, Lee YK, Jin CJ, Lee HJ, Hong CY, Ahn JS, Yang DH, Kim YK, Chung IJ, Park BC, Kim HJ, Lee JJ
    The major limitation for the maturation of dendritic cells (DCs) using Toll-like receptor (TLR) agonists is their decreased ability to migrate into lymph nodes compared with conventional DCs. CD38 can be used as a multifunctional marker to modulate migration, survival and Th1 responses of DCs. CD74 has been shown to negatively regulate DC migration. The goal of this study was to investigate the combinations of TLR agonists and interferons (IFNs) that most effectively regulate CD38 and CD74 expression on DCs. Synergistic TLR agonist stimulation in combination with IFN-α and IFN-γ was the best method for regulating CD38 and CD74 expression and inducing...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4638113</comments>
            <pubDate>Mon, 21 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4638113</guid>        </item>
        <item>
            <title>Low dosages: new chemotherapeutic weapons on the battlefield of immune-related disease.</title>
            <link>http://www.medworm.com/index.php?rid=4638112&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21423201%26dopt%3DAbstract</link>
            <description>Authors: Liu J, Zhao J, Hu L, Cao Y, Huang B
    Chemotherapeutic drugs eliminate tumor cells at relatively high doses and are considered weapons against tumors in clinics and hospitals. However, despite their ability to induce cellular apoptosis, chemotherapeutic drugs should probably be regarded more as a class of cell regulators than cell killers, if the dosage used and the fact that their targets are involved in basic molecular events are considered. Unfortunately, the regulatory properties of chemotherapeutic drugs are usually hidden or masked by the massive cell death induced by high doses. Recent evidence has begun to suggest that low dosages of chemotherapeutic drugs might profoundly regulate various intracellular aspects of normal cells, especially immune cells. Here, we discuss t...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4638112</comments>
            <pubDate>Mon, 21 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4638112</guid>        </item>
        <item>
            <title>Leptin in immuno-rheumatological diseases.</title>
            <link>http://www.medworm.com/index.php?rid=4638114&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21399656%26dopt%3DAbstract</link>
            <description>Authors: Vadacca M, Margiotta DP, Navarini L, Afeltra A
    Leptin is one of the most important hormones secreted by adipocytes, with a variety of physiological roles related to the control of metabolism and energy homeostasis. Since its discovery in 1994, leptin has attracted increasing interest in the scientific community for its pleiotropic actions. One of these functions is the relationship between nutritional status and immune competence. It structurally resembles proinflammatory cytokines, such as IL-6 and IL-12. The cytokine-like structural characteristic of leptin is implicative of its function in regulating immune responses. The role of leptin in regulating immune responses has been assessed in vitro as well as in clinical studies. It has been shown that disease conditions of redu...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4638114</comments>
            <pubDate>Mon, 14 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4638114</guid>        </item>
        <item>
            <title>Mannan-binding lectin directly interacts with Toll-like receptor 4 and suppresses lipopolysaccharide-induced inflammatory cytokine secretion from THP-1 cells.</title>
            <link>http://www.medworm.com/index.php?rid=4578906&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21383675%26dopt%3DAbstract</link>
            <description>Authors: Wang M, Chen Y, Zhang Y, Zhang L, Lu X, Chen Z
    Mannan-binding lectin (MBL) plays a key role in the lectin pathway of complement activation and can influence cytokine expression. Toll-like receptor 4 (TLR4) is expressed extensively and has been demonstrated to be involved in lipopolysaccharide (LPS)-induced signaling. We first sought to determine whether MBL exposure could modulate LPS-induced inflammatory cytokine secretion and nuclear factor-κB (NF-κB) activity by using the monocytoid cell line THP-1. We then investigated the possible mechanisms underlying any observed regulatory effect. Using ELISA and reverse transcriptase polymerase chain reaction (RT-PCR) analysis, we found that at both the protein and mRNA levels, treatment with MBL suppresses LPS-induced tumor-necrosi...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4578906</comments>
            <pubDate>Mon, 07 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4578906</guid>        </item>
        <item>
            <title>Altered influenza virus haemagglutinin (HA)-derived peptide is potent therapy for CIA by inducing Th1 to Th2 shift.</title>
            <link>http://www.medworm.com/index.php?rid=4578905&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21383676%26dopt%3DAbstract</link>
            <description>Authors: Sun J, Jia Y, Li R, Guo J, Sun X, Liu Y, Li Y, Yao H, Liu X, Zhao J, Li Z
    There has been an increase in interest in the use of altered peptides as antigen-specific therapeutic agents in autoimmune diseases. Here we investigated the inhibitory effect and possible mechanism of an altered influenza virus haemagglutinin (HA)-derived peptide in collagen-induced arthritis (CIA). CIA was induced in DBA/1 mice by immunisation with type II collagen (CII). Altered HA308-317, wild-type HA308-317 or irrelevant peptide was administered intranasally beginning from arthritis onset. Clinical and histological scores were assessed, and cytokine levels in the serum or supernatants from splenocytes were determined. The percentages of Th1 and Th2 cells in response to different peptides were analys...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4578905</comments>
            <pubDate>Mon, 07 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4578905</guid>        </item>
        <item>
            <title>IFN-α production by human mononuclear cells infected with varicella-zoster virus through TLR9-dependent and -independent pathways.</title>
            <link>http://www.medworm.com/index.php?rid=4578915&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21317915%26dopt%3DAbstract</link>
            <description>Authors: Yu HR, Huang HC, Kuo HC, Sheen JM, Ou CY, Hsu TY, Yang KD
    Understanding the defense mechanisms of the host of an organism is important for infection control. In previous studies, we demonstrated that interferon-α (IFN-α), but not IL-12, was produced by human peripheral blood mononuclear cells infected with varicella-zoster virus (VZV). Here, we investigated what kind of cell(s) and which signal molecule(s) are involved in IFN-α production. Using cell isolation and ELISA, we found that plasmacytoid dendritic cells (pDCs) were responsible for IFN-α production during VZV infection. We also found that Toll-like receptor 9 (TLR9) was involved in VZV-induced IFN-α production because inhibitory CpG oligodeoxynucleotide inhibited IFN-α production. UV-inactivated VZV-induced IFN-...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4578915</comments>
            <pubDate>Tue, 01 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4578915</guid>        </item>
        <item>
            <title>Celiac disease in patients with type 1 diabetes: a condition with distinct changes in intestinal immunity?</title>
            <link>http://www.medworm.com/index.php?rid=4578913&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21317917%26dopt%3DAbstract</link>
            <description>In this study, we investigated whether these characteristics were universal for CD independently of T1D association. For this purpose, we studied 36 children with normal small-bowel mucosa and 26 children with active CD, including 12 patients with T1D. In samples from the small-bowel mucosa, we detected the lowest expression of tight junction protein 1 (TJP1) mRNA in CD patients with T1D, indicating an increase in intestinal permeability. Furthermore, these samples displayed the highest expression of forkhead box P3 (FoxP3) mRNA, a marker for regulatory T cells, as compared with other patient groups. At the same time, serum levels of IgA antibodies specific for the CD-related antigens deamidated gliadin and tissue transglutaminase (tTG) were the highest in CD patients with T1D. In contrast...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4578913</comments>
            <pubDate>Tue, 01 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4578913</guid>        </item>
        <item>
            <title>Celiac disease: a model disease for gene-environment interaction.</title>
            <link>http://www.medworm.com/index.php?rid=4578912&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21317918%26dopt%3DAbstract</link>
            <description>Authors: Uibo R, Tian Z, Gershwin ME
    Celiac sprue remains a model autoimmune disease for dissection of genetic and environmental influences on disease progression. The 2010 Congress of Autoimmunity included several key sessions devoted to genetics and environment. Several papers from these symposia were selected for in-depth discussion and publication. This issue is devoted to this theme. The goal is not to discuss genetic and environmental interactions, but rather to focus on key elements of diagnosis, the inflammatory response and the mechanisms of autoimmunity.
    PMID: 21317918 [PubMed - in process] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4578912</comments>
            <pubDate>Tue, 01 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4578912</guid>        </item>
        <item>
            <title>A new algorithm for the diagnosis of celiac disease.</title>
            <link>http://www.medworm.com/index.php?rid=4578911&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21317919%26dopt%3DAbstract</link>
            <description>Authors: Rozenberg O, Lerner A, Pacht A, Grinberg M, Reginashvili D, Henig C, Barak M
    Celiac disease (CD) affects at least 1% of the Western population but remains largely unrecognized. In our laboratory, we utilize a novel algorithm to diagnose pediatric CD that offers both high sensitivity and high specificity for diagnosis in an outpatient setting. The aim of the present study was to challenge this algorithm and to test its performance in children and adults suspected of having CD. Using a three-assay algorithm, screening with the most sensitive tissue transglutaminase (tTG) complexed with deamidated gliadin peptide neoepitope immunoglobulin A (IgA)+IgG assay and confirming with the two specific tTG IgA and tTG IgA+IgG assays, we examined the serological results from 112 children ag...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4578911</comments>
            <pubDate>Tue, 01 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4578911</guid>        </item>
        <item>
            <title>Explosion of autoimmune diseases and the mosaic of old and novel factors.</title>
            <link>http://www.medworm.com/index.php?rid=4578910&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21358666%26dopt%3DAbstract</link>
            <description>Authors: Agmon-Levin N, Lian Z, Shoenfeld Y
    In recent decades, an enormous effort has been made to elucidate the pathogenesis of autoimmune and autoinflammatory diseases. Autoimmunity is a multifactorial process in which genetic, immunological, environmental and hormonal factors play in concert, together representing what was termed years ago the 'mosaic of autoimmunity'. To date, more than 80 systemic and organ-specific autoimmune diseases have been defined, and their cumulative burden is substantial, both medically and financially. Furthermore, the burden of autoimmune and autoinflammatory diseases is rising, making these diseases a ubiquitous global phenomenon that is predicted to further increase in the coming decades. In this issue of the journal, additional aspects of autoimmunit...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4578910</comments>
            <pubDate>Mon, 28 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4578910</guid>        </item>
        <item>
            <title>Marginal zone B cells are naturally reactive to collagen type II and are involved in the initiation of the immune response in collagen-induced arthritis.</title>
            <link>http://www.medworm.com/index.php?rid=4578909&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21358667%26dopt%3DAbstract</link>
            <description>Authors: Carnrot C, Prokopec KE, Råsbo K, Karlsson MC, Kleinau S
    Antibodies against type II collagen (CII) are essential for development of collagen-induced arthritis (CIA), but how and where the B-cell response to CII is initiated is not fully known. We show here that naive DBA/1 mice display naturally reactive IgM and IgG anti-CII producing B cells prior to immunization. The CII-reactive B cells were observed in the spleen and recognized as marginal zone (MZ) B cells. After CII immunization, CII-specific B cells expanded rapidly in the spleen, in contrast to the lymph nodes, with the initial response derived from MZ B cells and later by follicular (FO) B cells. This was evident despite that the MZ B cells were subject to stringent tolerance mechanisms by having a greater Fc gamma re...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4578909</comments>
            <pubDate>Mon, 28 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4578909</guid>        </item>
        <item>
            <title>Monte Carlo study of B-cell receptor clustering mediated by antigen crosslinking and directed transport.</title>
            <link>http://www.medworm.com/index.php?rid=4578908&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21358668%26dopt%3DAbstract</link>
            <description>Authors: Srinivas Reddy A, Tsourkas PK, Raychaudhuri S
    It is known from experiments that in the presence of soluble antigen, B-cell receptors (BCRs) assemble into microclusters and then collect into a macrocluster known as a 'cap'. However, the mechanisms of BCR cluster formation during recognition of soluble antigens remain unclear. In previous work, we demonstrated that effective intrinsic attractions among BCRs can lead to the formation of small microclusters of BCR molecules. The effective intrinsic attractions could be caused by multivalent antigen binding, association with lipid rafts, or other biochemical factors. In the present study, we have developed and studied a Monte Carlo model of BCR clustering mediated by explicit binding and crosslinking of soluble bivalent antigens. A...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4578908</comments>
            <pubDate>Mon, 28 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4578908</guid>        </item>
        <item>
            <title>Cytokine gene polymorphisms and graft-versus-host disease in children after matched sibling hematopoietic stem cell transplantation: a single-center experience.</title>
            <link>http://www.medworm.com/index.php?rid=4578907&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21358669%26dopt%3DAbstract</link>
            <description>Authors: Goussetis E, Varela I, Peristeri I, Kitra V, Spanou K, Moraloglou O, Paisiou A, Karatasaki S, Soldatou A, Constantinidou N, Graphakos S
    Various polymorphisms in cytokine genes have recently been investigated as candidate risk factors in allogeneic hematopoetic stem cell transplantation (allo-HSCT). We retrospectively analyzed specific polymorphisms in genes for interleukin (IL)-10, IL-6, tumor-necrosis factor alpha (TNF-α) and interferon gamma (IFN-γ) in a pediatric cohort of 57 histocompatibility leucocyte antigen (HLA)-identical sibling myeloablative transplants. Both recipient and donor genotypes were tested for association with graft-versus-host disease (GVHD) by statistical methods including Cox regression analysis. We found a significant association between the IL-10 p...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4578907</comments>
            <pubDate>Mon, 28 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4578907</guid>        </item>
        <item>
            <title>Thymoma and autoimmunity.</title>
            <link>http://www.medworm.com/index.php?rid=4578914&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21317916%26dopt%3DAbstract</link>
            <description>Authors: Shelly S, Agmon-Levin N, Altman A, Shoenfeld Y
    The thymus is a central lymphatic organ that is responsible for many immunological functions, including the production of mature, functional T cells and the induction of self-tolerance. Benign or malignant tumors may originate from the thymus gland, with thymoma being the most common and accounting for 50% of anterior mediastinal tumors. Malignancies linked to thymoma include the loss of self-tolerance and the presence of autoimmunity. In this review, we compiled the current scientific evidence detailing the various interactions between thymoma and autoimmune diseases, including myasthenia gravis, systemic lupus erythematosus, inappropriate antidiuretic hormone secretion, pure red cell aplasia, pernicious anemia, pemphigus and aut...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4578914</comments>
            <pubDate>Mon, 14 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4578914</guid>        </item>
        <item>
            <title>The role of gut microbiota (commensal bacteria) and the mucosal barrier in the pathogenesis of inflammatory and autoimmune diseases and cancer: contribution of germ-free and gnotobiotic animal models of human diseases.</title>
            <link>http://www.medworm.com/index.php?rid=4470750&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21278760%26dopt%3DAbstract</link>
            <description>Authors: Tlaskalová-Hogenová H, Stěpánková R, Kozáková H, Hudcovic T, Vannucci L, Tučková L, Rossmann P, Hrnčíř T, Kverka M, Zákostelská Z, Klimešová K, Přibylová J, Bártová J, Sanchez D, Fundová P, Borovská D, Srůtková D, Zídek Z, Schwarzer M, Drastich P, Funda DP
    Metagenomic approaches are currently being used to decipher the genome of the microbiota (microbiome), and, in parallel, functional studies are being performed to analyze the effects of the microbiota on the host. Gnotobiological methods are an indispensable tool for studying the consequences of bacterial colonization. Animals used as models of human diseases can be maintained in sterile conditions (isolators used for germ-free rearing) and specifically colonized with defined microbes (including non-...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4470750</comments>
            <pubDate>Mon, 31 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4470750</guid>        </item>
        <item>
            <title>Vitamin D and autoimmune thyroid diseases.</title>
            <link>http://www.medworm.com/index.php?rid=4470749&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21278761%26dopt%3DAbstract</link>
            <description>Authors: Kivity S, Agmon-Levin N, Zisappl M, Shapira Y, Nagy EV, Dankó K, Szekanecz Z, Langevitz P, Shoenfeld Y
    The role of vitamin D as an immune modulator has been emphasized in recent years, and low levels of the hormone were observed in several autoimmune diseases including multiple sclerosis and systemic lupus erythematosus. Vitamin D mediates its effect though binding to vitamin D receptor (VDR), and activation of VDR-responsive genes. While VDR gene polymorphism was found to associate with autoimmune thyroid diseases (AITDs), few studies examined levels of vitamin D in these patients and those that did yielded conflicting results. We therefore undertook to evaluate the levels of vitamin D in patients with AITDs compared to patients with non-AITDs and healthy controls. Serum vit...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4470749</comments>
            <pubDate>Mon, 31 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4470749</guid>        </item>
        <item>
            <title>The effects of Spirulina on anemia and immune function in senior citizens.</title>
            <link>http://www.medworm.com/index.php?rid=4470748&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21278762%26dopt%3DAbstract</link>
            <description>Authors: Selmi C, Leung PS, Fischer L, German B, Yang CY, Kenny TP, Cysewski GR, Gershwin ME
    Anemia and immunological dysfunction (i.e. immunosenescence) are commonly found in older subjects and nutritional approaches are sought to counteract these phenomena. Spirulina is a filamentous and multicellular bule-green alga capable of reducing inflammation and also manifesting antioxidant effects. We hypothesized that Spirulina may ameliorate anemia and immunosenescence in senior citizens with a history of anemia. We enrolled 40 volunteers of both sexes with an age of 50 years or older who had no history of major chronic diseases. Participants took a Spirulina supplementation for 12 weeks and were administered comprehensive dietary questionnaires to determine their nutritional regimen durin...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4470748</comments>
            <pubDate>Mon, 31 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4470748</guid>        </item>
        <item>
            <title>Celiac disease: diagnostic criteria in progress.</title>
            <link>http://www.medworm.com/index.php?rid=4470747&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21278763%26dopt%3DAbstract</link>
            <description>Authors: Volta U, Villanacci V
    Until a few years ago, celiac disease (CD) was thought to be a rare food intolerance that was confined to childhood and characterized by severe malabsorption and flat intestinal mucosa. Currently, CD is regarded as an autoimmune disorder that is common in the general population (affecting 1 in 100 individuals), with possible onset at any age and with many possible presentations. The identification of CD is challenging because it can begin not only with diarrhea and weight loss but also with atypical gastrointestinal (constipation and recurrent abdominal pain) and extra-intestinal symptoms (anemia, raised transaminases, osteoporosis, recurrent miscarriages, aphthous stomatitis and associated autoimmune disorders), or it could be completely symptomless. Ove...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4470747</comments>
            <pubDate>Mon, 31 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4470747</guid>        </item>
        <item>
            <title>Immunostimulation in the era of the metagenome.</title>
            <link>http://www.medworm.com/index.php?rid=4470746&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21278764%26dopt%3DAbstract</link>
            <description>Authors: Proal AD, Albert PJ, Blaney GP, Lindseth IA, Benediktsson C, Marshall TG
    Microbes are increasingly being implicated in autoimmune disease. This calls for a re-evaluation of how these chronic inflammatory illnesses are routinely treated. The standard of care for autoimmune disease remains the use of medications that slow the immune response, while treatments aimed at eradicating microbes seek the exact opposite-stimulation of the innate immune response. Immunostimulation is complicated by a cascade of sequelae, including exacerbated inflammation, which occurs in response to microbial death. Over the past 8 years, we have collaborated with American and international clinical professionals to research a model-based treatment for inflammatory disease. This intervention, designed t...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4470746</comments>
            <pubDate>Mon, 31 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4470746</guid>        </item>
        <item>
            <title>Novel trends in celiac disease.</title>
            <link>http://www.medworm.com/index.php?rid=4470745&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21278765%26dopt%3DAbstract</link>
            <description>Authors: Matthias T, Neidhöfer S, Pfeiffer S, Prager K, Reuter S, Gershwin ME
    Celiac disease (CD) is one of the most common food intolerances in developed world. It affects genetically susceptible individuals and has severe consequences if it remains undiagnosed. A disease known for more than a century, it is still the focus for experts from various fields of research and development. Geneticists, pathologists, immunologists, food engineers and dieticians share their knowledge and expertise to improve the conditions of CD patients. With new insights in the pathomechanism of gluten processing and antigen presentation in CD, it was possible to improve the diagnostic antigen mimicking the primary epitope in CD. These celiac neo-epitopes are comprised of a complex of gliadin peptides cros...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4470745</comments>
            <pubDate>Mon, 31 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4470745</guid>        </item>
        <item>
            <title>The epigenetics of autoimmunity.</title>
            <link>http://www.medworm.com/index.php?rid=4470744&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21278766%26dopt%3DAbstract</link>
            <description>Authors: Meda F, Folci M, Baccarelli A, Selmi C
    The etiology of autoimmune diseases remains largely unknown. Concordance rates in monozygotic twins are lower than 50% while genome-wide association studies propose numerous significant associations representing only a minority of patients. These lines of evidence strongly support other complementary mechanisms involved in the regulation of genes expression ultimately causing overt autoimmunity. Alterations in the post-translational modification of histones and DNA methylation are the two major epigenetic mechanisms that may potentially cause a breakdown of immune tolerance and the perpetuation of autoimmune diseases. In recent years, several studies both in clinical settings and experimental models proposed that the epigenome may hold th...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4470744</comments>
            <pubDate>Mon, 31 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4470744</guid>        </item>
        <item>
            <title>Dysfunctions of the Iga system: a common link between intestinal and renal diseases.</title>
            <link>http://www.medworm.com/index.php?rid=4470743&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21278767%26dopt%3DAbstract</link>
            <description>Authors: Papista C, Berthelot L, Monteiro RC
    Immunoglobulin A (Iga)-isotype antibodies play an important role in immunity owing to their structure, glycosylation, localization and receptor interactions. Dysfunctions in this system can lead to multiple types of pathology. This review describes the characteristics of Iga and discusses the involvement of abnormalities in the Iga system on the development of celiac disease and Iga nephropathy.Cellular &amp; Molecular Immunology advance online publication, 31 January 2011; doi:10.1038/cmi.2010.69.
    PMID: 21278767 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4470743</comments>
            <pubDate>Mon, 31 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4470743</guid>        </item>
        <item>
            <title>Antibodies in celiac disease: implications beyond diagnostics.</title>
            <link>http://www.medworm.com/index.php?rid=4470742&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21278768%26dopt%3DAbstract</link>
            <description>Authors: Caja S, Mäki M, Kaukinen K, Lindfors K
    Celiac disease is a multisystemic dietary, gluten-induced autoimmune disorder characterized by the presence of transglutaminase (TG) 2 serum autoantibodies. Distinct autoantibodies targeting members of the TG family (TG2, TG3 and TG6) are found deposited in small-bowel mucosa and in extraintestinal tissues affected by the disease. Serum autoantibodies against other self-antigens also emerge in untreated celiac disease patients. Although villous atrophy and crypt hyperplasia in small-bowel biopsy samples are still the gold standards in diagnostics, celiac disease-specific antibodies are widely used as diagnostic aids. Gluten-induced small-bowel mucosal T-cell response is the cornerstone in the pathogenesis of the disorder, but humoral imm...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4470742</comments>
            <pubDate>Mon, 31 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4470742</guid>        </item>
        <item>
            <title>The inflammasomes in health and disease: from genetics to molecular mechanisms of autoinflammation and beyond.</title>
            <link>http://www.medworm.com/index.php?rid=4400440&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21258359%26dopt%3DAbstract</link>
            <description>Authors: Conforti-Andreoni C, Ricciardi-Castagnoli P, Mortellaro A
    Nucleotide-binding oligomerization domain (NOD)-containing protein-like receptors (NLRs) are a recently discovered class of innate immune receptors that play a crucial role in initiating the inflammatory response following pathogen recognition. Some NLRs form the framework for cytosolic platforms called inflammasomes, which orchestrate the early inflammatory process via IL-1β activation. Mutations and polymorphisms in NLR-coding genes or in genetic loci encoding inflammasome-related proteins correlate with a variety of autoinflammatory diseases. Moreover, the activity of certain inflammasomes is associated with susceptibility to infections as well as autoimmunity and tumorigenesis. In this review, we will discuss how i...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4400440</comments>
            <pubDate>Mon, 24 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4400440</guid>        </item>
        <item>
            <title>Application of a novel inhibitor of human CD59 for the enhancement of complement-dependent cytolysis on cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=4400439&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21258360%26dopt%3DAbstract</link>
            <description>Authors: You T, Hu W, Ge X, Shen J, Qin X
    Many monoclonal antibodies (mAbs) have been extensively used in the clinic, such as rituximab to treat lymphoma. However, resistance and non-responsiveness to mAb treatment have been challenging for this line of therapy. Complement is one of the main mediators of antibody-based cancer therapy via the complement-dependent cytolysis (CDC) effect. CD59 plays a critical role in resistance to mAbs through the CDC effect. In this paper, we attempted to investigate whether the novel CD59 inhibitor, recombinant ILYd4, was effective in enhancing the rituximab-mediated CDC effect on rituximab-sensitive RL-7 lymphoma cells and rituximab-induced resistant RR51.2 cells. Meanwhile, the CDC effects, which were mediated by rituximab and anti-CD24 mAb, on the r...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4400439</comments>
            <pubDate>Mon, 24 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4400439</guid>        </item>
        <item>
            <title>Do viral infections protect from or enhance type 1 diabetes and how can we tell the difference?</title>
            <link>http://www.medworm.com/index.php?rid=4400438&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21258361%26dopt%3DAbstract</link>
            <description>Authors: Christen U, von Herrath MG
    Virus infections have been implicated in both initiation of and protection from autoimmune diseases, such as type 1 diabetes (T1D). In this review we intend to reflect on recent evidence how viruses might on the one hand be involved in the pathogenesis of T1D and on the other hand induce a state of protection from autoimmune-mediated damage. It is important to acknowledge that human individuals encounter more than just one virus infection in their lifetime. Therefore, it is important to integrate more than just one possible environmental triggering factor for autoimmune diseases to occur.Cellular &amp; Molecular Immunology advance online publication, 24 January 2011; doi:10.1038/cmi.2010.71.
    PMID: 21258361 [PubMed - as supplied by publisher] (Sou...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4400438</comments>
            <pubDate>Mon, 24 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4400438</guid>        </item>
        <item>
            <title>CD47: a new player in phagocytosis and xenograft rejection.</title>
            <link>http://www.medworm.com/index.php?rid=4400437&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21258362%26dopt%3DAbstract</link>
            <description>Authors: Navarro-Alvarez N, Yang YG
    Organ transplantation is limited by the availability of human donor organs. The transplantation of organs and tissues from other species (xenotransplantation) would supply an unlimited number of organs and offer many other advantages for which the pig has been identified as the most suitable source. However, the robust immune responses to xenografts remain a major obstacle to clinical application of xenotransplantation. The more vigorous xenograft rejection relative to allograft rejection is largely accounted for by the extensive genetic disparities between the donor and recipient. Xenografts activate host immunity not only by expressing immunogenic xenoantigens that provide the targets for immune recognition and rejection, but also by lacking ligand...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4400437</comments>
            <pubDate>Mon, 24 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4400437</guid>        </item>
        <item>
            <title>Pleural fluid from tuberculous pleurisy inhibits the functions of T cells and the differentiation of Th1 cells via immunosuppressive factors.</title>
            <link>http://www.medworm.com/index.php?rid=4400436&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21258363%26dopt%3DAbstract</link>
            <description>Authors: Li Q, Li L, Liu Y, Fu X, Qiao D, Wang H, Lao S, Huang F, Wu C
    Immunosuppressive mediators in tuberculosis pleurisy (pleural fluid (PF)) are associated with the course of disease, but they remain poorly defined. To study the local immune status of patients with tuberculosis pleurisy, we examined the effect of PF on the functions of T cells and the differentiation of Th1 cells. PF could inhibit the ability of T cells to produce cytokines. However, tumor-necrosis factor (TNF)-α derived from non-T cells was not impaired. Further analysis indicated that cell activation and cell cycle progression were also suppressed. Moreover, PF could inhibit Th1 cell differentiation. Importantly, we found that inhibitors of indoleamine 2,3-dioxygenase (IDO) and adenosine and neutralizing antibod...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4400436</comments>
            <pubDate>Mon, 24 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4400436</guid>        </item>
        <item>
            <title>TNFR2 expression on non-bone marrow-derived cells is crucial for lipopolysaccharide-induced septic shock and downregulation of soluble TNFR2 level in serum.</title>
            <link>http://www.medworm.com/index.php?rid=4400435&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21258364%26dopt%3DAbstract</link>
            <description>In this study, murine bone marrow (BM) chimeras selectively expressing TNFR2 on either BM-derived or non-BM-derived cells were generated and challenged with lipopolysaccharide (LPS). The results show that TNFR2 expression on non-BM-derived cells is crucial for both the sensitivity of mice to LPS and the downregulation of sTNFR2 in serum. Most importantly, sTNFR2 was released from both BM- and non-BM-derived cells. Non-BM TNFR1 expression influenced the sensitivity of mice to LPS challenge but not the level of serum sTNFR2. These results provide the first in vivo evidence for the origin and regulation of sTNFR2 in serum and could aid in the development of novel anti-TNF strategies against septic shock.Cellular &amp; Molecular Immunology advance online publication, 24 January 2011; doi:10.10...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4400435</comments>
            <pubDate>Mon, 24 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4400435</guid>        </item>
        <item>
            <title>In situ mass spectrometry of autoimmune liver diseases.</title>
            <link>http://www.medworm.com/index.php?rid=4400434&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21258365%26dopt%3DAbstract</link>
            <description>Authors: Bowlus CL, Seeley EH, Roder J, Grigorieva J, Roder H, Caprioli RM, Gershwin M
    Primary biliary cirrhosis (PBC), primary sclerosing cholangitis (PSC) and autoimmune hepatitis (AIH) are the major forms of autoimmune liver diseases each characterized by the destruction of a specific liver cell type and the presence of differing auto-antibodies. We took a proteomic approach utilizing in situ matrix-assisted laser desorption/ionization mass spectrometry (MALDI MS) to obtain profiles directly from liver samples of patients with PBC, PSC, AIH and controls. The ability to precisely localize the region for acquisition of MALDI MS allowed us to obtain profiles from bile ducts, inflammatory infiltrates and hepatocytes from each biopsy sample. Analysis tools developed to identify peaks and...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4400434</comments>
            <pubDate>Mon, 24 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4400434</guid>        </item>
        <item>
            <title>4-1BB signaling beyond T cells.</title>
            <link>http://www.medworm.com/index.php?rid=4337164&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21217771%26dopt%3DAbstract</link>
            <description>Authors: Vinay DS, Kwon BS
    Originally discovered as a T cell-activating molecule, 4-1BB (CD137) is now also recognized as an activator of non-T cells, thus imparting a new dimension to its potential in vivo effects. 4-1BB expression is seen on a variety of non-T cells including activated dendritic cells (DCs), monocytes, neutrophils, B cells and natural killer (NK) cells, and promotes their individual effector functions. The T cell- and non-T cell-activating ability of 4-1BB may be the basis of its powerful anti-cancer, anti-autoimmune and anti-viral effects. Here we discuss the consequence and importance of 4-1BB signaling in non-T cells. We consider its effects on immune regulation, and the distinct and/or overlapping pathways involved in these responses, as well as possible therapeu...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4337164</comments>
            <pubDate>Mon, 10 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4337164</guid>        </item>
        <item>
            <title>Current progress in γδ T-cell biology.</title>
            <link>http://www.medworm.com/index.php?rid=4139599&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21042298%26dopt%3DAbstract</link>
            <description>Authors: Hao J, Wu X, Xia S, Li Z, Wen T, Zhao N, Wu Z, Wang P, Zhao L, Yin Z
    T lymphocytes bearing γ- and δ-chain T-cell receptor heterodimers are named γδ T cells. Interestingly, γδ and αβ T cells share the same progenitors, and they undergo a fate decision in the thymus. Functional differentiation of γδ T cells occurs both inside and outside the thymus. Antigen recognition of γδ T-cell receptors is very unique, and the responses frequently exhibit innate characteristics. Nevertheless, peripheral γδ T cells exert a number of effector and regulatory functions. γδ T cells rapidly produce cytokines like interferon (IFN)-γ and IL-17 and promote inflammation, partly due to the inherent epigenetic and transcriptional programs, which facilitates a quick and extensive respon...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4139599</comments>
            <pubDate>Mon, 01 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4139599</guid>        </item>
        <item>
            <title>Identification of p100 target promoters by chromatin immunoprecipitation-guided ligation and selection (ChIP-GLAS).</title>
            <link>http://www.medworm.com/index.php?rid=4042925&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20921938%26dopt%3DAbstract</link>
            <description>Authors: Liu X, Dong L, Zhang X, Wang B, Wang X, Li H, He J, Ge L, Jing X, Yao Z, Yang J
    The multifunctional protein p100 is a vital transcriptional regulator that increases gene transcription by forming a physical bridge between promoter-specific transcription factors and the basal transcription machinery. To identify potential signal transduction pathways in which human p100 acts as a coregulator and to find target promoter regions that may interact with p100, we performed a promoter microarray assay called chromatin immunoprecipitation-guided ligation and selection (ChIP-GLAS). From this assay, we determined that a set of promoter fragments, including several factors in the transforming growth factor beta (TGF-β) signaling pathway, exhibited interaction with p100. The ChIP-GLAS dat...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4042925</comments>
            <pubDate>Sun, 03 Oct 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4042925</guid>        </item>
        <item>
            <title>Enhancing the antihepatitis B virus immune response by adefovir dipivoxil and entecavir therapies.</title>
            <link>http://www.medworm.com/index.php?rid=4042924&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20921939%26dopt%3DAbstract</link>
            <description>In this study, regulatory T cells (Tregs) and intracellular cytokines, including IL-2, interferon (IFN)-γ, tumor-necrosis factor (TNF)-α and IL-4, were measured prior to and at 12, 24, 36 and 48 weeks after treatment with ETV or ADV. The cytokines were increased from 24 to 48 weeks after treatment. Higher levels of Th1 cytokines were observed with ETV (n=29) versus ADV (n=28) treatment. By contrast, the numbers of Tregs in both groups were decreased. The altered cytokine profile and cellular component was accompanied by a decrease in HBV DNA levels in both groups, which may contribute to their therapeutic effect in CHB infection. Our findings suggest that the antiviral effect of the drugs may be attributed not only to their direct effect on virus suppression but also to their immunoregul...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4042924</comments>
            <pubDate>Sun, 03 Oct 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4042924</guid>        </item>
        <item>
            <title>Pathway-selective suppression of chemokine receptor signaling in B cells by LPS through downregulation of PLC-Î²2.</title>
            <link>http://www.medworm.com/index.php?rid=4003928&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20871625%26dopt%3DAbstract</link>
            <description>Authors: Shirakawa AK, Liao F, Zhang HH, Hedrick MN, Singh SP, Wu D, Farber JM
    Lymphocyte activation leads to changes in chemokine receptor expression. There are limited data, however, on how lymphocyte activators can alter chemokine signaling by affecting downstream pathways. We hypothesized that B cell-activating agents might alter chemokine responses by affecting downstream signal transducers, and that such effects might differ depending on the activator. We found that activating mouse B cells using either anti-IgM or lipopolysaccharide (LPS) increased the surface expression of CCR6 and CCR7 with large increases in chemotaxis to their cognate ligands. By contrast, while anti-IgM also led to enhanced calcium responses, LPS-treated cells showed only small changes in calcium signaling ...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4003928</comments>
            <pubDate>Sun, 26 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4003928</guid>        </item>
        <item>
            <title>Induction of antitumor immunity against mouse carcinoma by baculovirus-infected dendritic cells.</title>
            <link>http://www.medworm.com/index.php?rid=4003854&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20871626%26dopt%3DAbstract</link>
            <description>In this study, we evaluated the induction of antitumor immunity in mice by baculovirus-infected BMDCs against lung cancer and melanoma. After treatment with baculovirus-infected BMDCs, murine lung tumors caused by Lewis lung carcinoma (LLC) cells were significantly reduced in size, and the survival of the mice was improved. In addition, experiments using a melanoma mouse model showed that baculovirus-infected BMDCs inhibited tumor growth and improved survival compared with controls. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and creatinine levels remained normal in baculovirus-infected BMDC-treated mice. Our findings show that baculovirus-infected DCs induce antitumor immunity and pave the way for the use of this technique as an effective tool for DC immunothera...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4003854</comments>
            <pubDate>Sun, 26 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4003854</guid>        </item>
        <item>
            <title>Immobilized MHC class I chain-related protein A synergizes with IL-15 and soluble 4-1BB ligand to expand NK cells with high cytotoxicity ex vivo.</title>
            <link>http://www.medworm.com/index.php?rid=4003761&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20871627%26dopt%3DAbstract</link>
            <description>In this study, we showed that recombinant, immobilized MICA (iMICA) molecules coated on plastic wells weakly promote peripheral NK cell activation, secretion of interferon (IFN)-Î³ and degranulation without inducing apoptosis. In addition, iMICA synergized with IL-15 and soluble 4-1BB ligand (s4-1BBL) to expand NK cells 25- to 42-fold in a 13-day culture, whereas NK cells stimulated only with IL-15 and s4-1BBL expanded 10- to 16-fold. In contrast to NK cells expanded by IL-15 and s4-1BBL stimulation, NK cells expanded long term in the presence of iMICA exhibited increased cytotoxicity against leukemia cells. These results suggest that large numbers of NK cells with high cytotoxicity can be generated by stimulation with IL-15 and s4-1BBL in the presence of iMICA and that these cells can b...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4003761</comments>
            <pubDate>Sun, 26 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4003761</guid>        </item>
        <item>
            <title>2-Gy whole-body irradiation significantly alters the balance of CD4(+)CD25(- )T effector cells and CD4(+)CD25(+)Foxp3(+ )T regulatory cells in mice.</title>
            <link>http://www.medworm.com/index.php?rid=4003560&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20871628%26dopt%3DAbstract</link>
            <description>Authors: Qu Y, Zhang B, Liu S, Zhang A, Wu T, Zhao Y
    CD4(+)CD25(+) T regulatory (Treg) cells are critical in inducing and maintaining immunological self-tolerance as well as transplant tolerance. The effect of low doses of whole-body irradiation (WBI) on CD4(+)CD25(+)Foxp3(+) Treg cells has not been determined. The proportion, phenotypes and function of CD4(+)CD25(+) Treg cells were investigated 0.5, 5 and 15 days after euthymic, thymectomized or allogeneic bone marrow transplanted C57BL/6 mice received 2-Gy Î³-rays of WBI. The 2-Gy WBI significantly enhanced the ratios of CD4(+)CD25(+) Treg cells and CD4(+)CD25(+)Foxp3(+) Treg cells to CD4(+) T cells in peripheral blood, lymph nodes, spleens and thymi of mice. The CD4(+)CD25(+) Treg cells of the WBI-treated mice showed immunosuppres...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4003560</comments>
            <pubDate>Sun, 26 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4003560</guid>        </item>
        <item>
            <title>IL-15 increases the frequency of effector memory CD8(+) T cells in rhesus monkeys immunized with HIV vaccine.</title>
            <link>http://www.medworm.com/index.php?rid=4003523&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20871629%26dopt%3DAbstract</link>
            <description>Authors: Li S, Qi X, Gao Y, Hao Y, Cui L, Ruan L, He W
    Several studies have suggested that interleukin (IL)-15 is a promising adjuvant that promotes cellular immunity when administered with human immunodeficiency virus (HIV) vaccine. Here we evaluated the effect of IL-15 plasmid on HIV-specific immune responses, especially cellular immunity, in eight rhesus monkeys. These monkeys were immunized three times with HIV DNA vaccine with or without IL-15 plasmid and boosted with recombinant Tiantan strain vaccinia virus-based HIV vaccine (rTV) 22 weeks after the first immunization. Although we did not detect any significant differences in the HIV-specific CD8(+) T-cell response between monkeys with IL-15 coimmunization and monkeys with HIV vaccine alone, our results showed that the frequency...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4003523</comments>
            <pubDate>Sun, 26 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4003523</guid>        </item>
        <item>
            <title>Loss of microRNAs in thymus perturbs invariant NKT cell development and function.</title>
            <link>http://www.medworm.com/index.php?rid=3987886&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20852654%26dopt%3DAbstract</link>
            <description>Authors: Seo KH, Zhou L, Meng D, Xu J, Dong Z, Mi QS
    microRNAs (miRNAs) are small noncoding RNAs that mediate RNA interference to suppress protein expression at the translational level. Accumulated evidence indicates that miRNAs play critical roles in various biological processes and disease development, including autoimmune diseases. Invariant natural killer T (iNKT) cells are an unusual CD1d-restricted subset of thymus-derived T cells that are potent regulators of diverse immune responses. Our previous studies with the mouse model of bone marrow-specific Dicer deletion suggest the involvement of Dicer-dependent miRNAs in the development and function of iNKT cells. In the present study, to further dissect the functional levels of Dicer-dependent miRNAs in regulating iNKT cell developm...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3987886</comments>
            <pubDate>Sun, 19 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3987886</guid>        </item>
        <item>
            <title>Non-hematopoietic cells contribute to protective tolerance to Aspergillus fumigatus via a TRIF pathway converging on IDO.</title>
            <link>http://www.medworm.com/index.php?rid=3981464&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20835271%26dopt%3DAbstract</link>
            <description>Authors: de Luca A, Bozza S, Zelante T, Zagarella S, D'Angelo C, Perruccio K, Vacca C, Carvalho A, Cunha C, Aversa F, Romani L
    Innate responses combine with adaptive immunity to generate the most effective form of anti-Aspergillus immune resistance. Whereas the pivotal role of dendritic cells in determining the balance between immunopathology and protective immunity to the fungus is well established, we determined that epithelial cells (ECs) also contributes to this balance. Mechanistically, EC-mediated protection occurred through a Toll-like receptor 3/Toll/IL-1 receptor domain-containing adaptor-inducing interferon (TLR3/TRIF)-dependent pathway converging on indoleamine 2,3-dioxygenase (IDO) via non-canonical nuclear factor-ÎºB activation. Consistent with the high susceptibility of...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3981464</comments>
            <pubDate>Sun, 12 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3981464</guid>        </item>
        <item>
            <title>Contribution of functional KIR3DL1 to ankylosing spondylitis.</title>
            <link>http://www.medworm.com/index.php?rid=3954769&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20818412%26dopt%3DAbstract</link>
            <description>Authors: Zvyagin IV, Mamedov IZ, Britanova OV, Staroverov DB, Nasonov EL, Bochkova AG, Chkalina AV, Kotlobay AA, Korostin DO, Rebrikov DV, Lukyanov S, Lebedev YB, Chudakov DM
    Increasing evidence points to a role for killer immunoglobulin-like receptors (KIRs) in the development of autoimmune diseases. In particular, a positive association of KIR3DS1 (activating receptor) and a negative association of KIR3DL1 (inhibitory receptor) alleles with ankylosing spondylitis (AS) have been reported by several groups. However, none of the studies analyzed these associations in the context of functionality of polymorphic KIR3DL1. To better understand how the KIR3DL1/3DS1 genes determine susceptibility to AS, we analyzed the frequencies of alleles and genotypes encoding functional (KIR3DL1*F) and n...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3954769</comments>
            <pubDate>Sun, 05 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3954769</guid>        </item>
        <item>
            <title>Cellular &amp; Molecular Immunology receives its first Impact Factor.</title>
            <link>http://www.medworm.com/index.php?rid=3954770&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20818411%26dopt%3DAbstract</link>
            <description>Authors: Tian Z
    
    PMID: 20818411 [PubMed - in process] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3954770</comments>
            <pubDate>Tue, 31 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3954770</guid>        </item>
        <item>
            <title>Antigen-non-specific regulation centered on CD25(+)Foxp3(+) Treg cells.</title>
            <link>http://www.medworm.com/index.php?rid=3912043&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20729905%26dopt%3DAbstract</link>
            <description>Authors: Hu G, Liu Z, Zheng C, Zheng SG
    CD4(+)CD25(+)Foxp3(+) regulatory T cells (Tregs) are of special interest in immunology because of their potent inhibitory function. Many fundamental aspects of Tregs, including their antigenic profile, development and peripheral homeostasis, remain highly controversial. Here, we propose a Treg-centered antigen-non-specific immunoregulation model focused on the T-cell system, particularly on CD4(+) T cells. The T-cell pool consists of naive T cells (Tnais), Tregs and effector T cells (Teffs). Regardless of antigen specificity, the ratio of the activated T-cell subsets (Treg/Teff/Tnai) and their temporal and spatial uniformity dictate the differentiation of Tnais. Activated Tregs inhibit the activation, proliferation, induction and activity of Teff...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3912043</comments>
            <pubDate>Sun, 22 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3912043</guid>        </item>
        <item>
            <title>CD4(+)CD25(+) but not CD4(+)Foxp3(+) T cells as a regulatory subset in primary biliary cirrhosis.</title>
            <link>http://www.medworm.com/index.php?rid=3912042&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20729906%26dopt%3DAbstract</link>
            <description>This study was undertaken to investigate Tregs and different cytokines in the liver and peripheral blood of PBC patients. We found that these patients demonstrated a reduction of CD4(+)CD25(+) T cells but elevated CD4(+)Foxp3(+) T cells in peripheral blood mononuclear cells (PBMCs) and CD4(+) T cells. The percentage of CD4(+)CD25(+) T cells in PBMCs was negatively correlated with elevated plasma interferon (IFN)-gamma levels. A liver-specific analysis showed that the frequency of Foxp3(+) Tregs, transforming growth factor (TGF)-beta1 and IFN-gamma were increased in PBC patients. Our findings suggest that an imbalance between CD4(+)CD25(+) Tregs and cytotoxic cytokines plays a crucial role in the pathogenesis of PBC while the role of Foxp3 needs further investigation.Cellular &amp; Molecula...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3912042</comments>
            <pubDate>Sun, 22 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3912042</guid>        </item>
        <item>
            <title>Natural killer cell-triggered vascular transformation: maternal care before birth?</title>
            <link>http://www.medworm.com/index.php?rid=3882108&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20711229%26dopt%3DAbstract</link>
            <description>Authors: Zhang J, Chen Z, Smith GN, Croy BA
    Natural killer (NK) cells are found in lymphoid and non-lymphoid organs. In addition to important roles in immune surveillance, some NK cells contribute to angiogenesis and circulatory regulation. The uterus of early pregnancy is a non-lymphoid organ enriched in NK cells that are specifically recruited to placental attachment sites. In species with invasive hemochorial placentation, these uterine natural killer (uNK) cells, via secretion of cytokines, chemokines, mucins, enzymes and angiogenic growth factors, contribute to the physiological change of mesometrial endometrium into the unique stromal environment called decidua basalis. In humans, uNK cells have the phenotype CD56(bright)CD16(dim) and they appear in great abundance in the late se...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3882108</comments>
            <pubDate>Sun, 15 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3882108</guid>        </item>
        <item>
            <title>Hepatitis B virus X protein suppresses virus-triggered IRF3 activation and IFN-beta induction by disrupting the VISA-associated complex.</title>
            <link>http://www.medworm.com/index.php?rid=3882107&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20711230%26dopt%3DAbstract</link>
            <description>Authors: Wang X, Li Y, Mao A, Li C, Li Y, Tien P
    Viral RNAs produced during viral infection are recognized by the cytoplasmic RNA helicases retinoic acid-inducible gene-I (RIG-I) and melanoma differentiation-associated gene 5 (MDA5). A central adapter protein downstream of RIG-I and MDA5 is the mitochondrial membrane protein virus-induced signaling adaptor (VISA), which mediates the induction of type I interferons (IFNs) through the activation of transcription factors such as nuclear factor-kappaB (NF-kappaB) and IFN-regulatory factor-3 (IRF3). Here we found that hepatitis B virus (HBV)-encoded X protein (HBx) acts as an inhibitor of virus-triggered IRF3 activation and IFN-beta induction. Reporter and plaque assays indicate that HBx inhibits signaling by components upstream but not dow...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3882107</comments>
            <pubDate>Sun, 15 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3882107</guid>        </item>
        <item>
            <title>Hepatitis B-specific T helper cell responses in uninfected infants born to HBsAg(+)/HBeAg(-) mothers.</title>
            <link>http://www.medworm.com/index.php?rid=3791640&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20657604%26dopt%3DAbstract</link>
            <description>This study was undertaken to investigate HBV antigen-specific T-cell responses in vaccinated neonates of HBsAg(+)/HBeAg(-) mothers. Blood was collected from 46 HBsAg(+) mothers and their neonates (subjects) as well as 24 age-matched controls. All neonates of HBsAg(+) mothers received appropriate immunoprophylaxis, and HBsAg and hepatitis B surface antibody (anti-HBs) antibody titers were determined after completion of the vaccination course. Peripheral blood mononuclear cells (PBMCs) from infants at birth, 1 and 6 months of age were stimulated with recombinant HBsAg, hepatitis B core antigen (HBcAg) and mitogen, and interferon (IFN)-gamma concentrations were determined by ELISA. HBsAg-induced production of IL-2, IL-5, IL-6 and IL-10 was assessed using a cytometric bead array kit on cells f...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3791640</comments>
            <pubDate>Sun, 25 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3791640</guid>        </item>
        <item>
            <title>Identification of two aberrant transcripts derived from a hybridoma with amplification of functional immunoglobulin variable genes.</title>
            <link>http://www.medworm.com/index.php?rid=3791639&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20657605%26dopt%3DAbstract</link>
            <description>In this study, we report the detection of two aberrant transcripts from a hybridoma produced using myeloma cell line OUR-1, the development of a method to distinguish between the functional and abundant aberrant V(L) transcripts, and the origins of these aberrant genes. The aberrant V(L) gene is derived from OUR-1 cells, while the aberrant V(H) gene might derive from antibody repertoires in B cells or from gene rearrangement in the hybridoma cells. The aberrant V(H) and V(L) genes in this study may facilitate discrimination between the functional and aberrant variable genes from hybridoma cells.Cellular &amp; Molecular Immunology advance online publication, 26 July 2010; doi:10.1038/cmi.2010.33.
    PMID: 20657605 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Immunolo...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3791639</comments>
            <pubDate>Sun, 25 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3791639</guid>        </item>
        <item>
            <title>Type 1 T-cell responses in chlamydial lung infections are associated with local MIP-1alpha response.</title>
            <link>http://www.medworm.com/index.php?rid=3758997&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20622889%26dopt%3DAbstract</link>
            <description>Authors: Zhang N, Wang Z, Tang X, Wang H, Li H, Huang H, Bai H, Yang X
    Chemokines and their receptors are important mediators of leukocyte trafficking and recruitment and sometimes work as modulators of T-cell responses during infections and inflammation. Modulating the biological activity of chemokines has been found to influence the course of diseases. However, little is known about the role of chemokine responses during chlamydial lung infections. We therefore analyzed the dynamics of multiple chemokines, which are frequently associated with type 1 (Th1) T cell immune responses, and their receptors for their expression in the lungs during Chlamydia muridarum (Cm) infections. We also examined the relationship between chemokine responses and the development of Th1 responses as well as...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3758997</comments>
            <pubDate>Sun, 11 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3758997</guid>        </item>
        <item>
            <title>Restoration of dysregulated CC chemokine signaling for monocyte/macrophage chemotaxis in head and neck squamous cell carcinoma patients by neem leaf glycoprotein maximizes tumor cell cytotoxicity.</title>
            <link>http://www.medworm.com/index.php?rid=3758996&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20622890%26dopt%3DAbstract</link>
            <description>Authors: Chakraborty K, Bose A, Chakraborty T, Sarkar K, Goswami S, Pal S, Baral R
    Previous studies have shown that the CC chemokine receptor CCR5 is downregulated on monocyte/macrophage (MO/Mphi) surfaces in head and neck squamous cell carcinoma (HNSCC) patients (stage IIIB). Ligands (RANTES, MIP-1alpha and MIP-1beta) of this chemokine receptor were also secreted in lesser quantity from MO/Mphi of HNSCC patients in comparison with healthy individuals. In an aim to restore this dysregulated receptor-ligand signaling, we have used neem leaf glycoprotein (NLGP), a novel immunomodulator reported from our laboratory. NLGP upregulated CCR5 expression, as evidenced from studies on MO/Mphi of peripheral blood from HNSCC patients as well as healthy individuals. Expression of RANTES, MIP-1alpha...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3758996</comments>
            <pubDate>Sun, 11 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3758996</guid>        </item>
        <item>
            <title>Murine lung eosinophil activation and chemokine production in allergic airway inflammation.</title>
            <link>http://www.medworm.com/index.php?rid=3758995&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20622891%26dopt%3DAbstract</link>
            <description>In this study, the properties and functions of homeostatic and activated eosinophils were compared. Eosinophils from normal tissues expressed costimulation and adhesion molecules B7-1, B7-2 and ICAM-1 for Ag presentation but little major histocompatibility complex (MHC) class II, and were found to be poor stimulators of T-cell proliferation. However, these eosinophils expressed high levels of chemokine mRNA including C10, macrophage inflammatory protein (MIP)-1alpha, MIP-1gamma, MIP-2, eotaxin and monocyte chemoattractant protein-5 (MCP-5), and produced chemokine proteins. Eosinophil intracellular chemokines decreased rapidly with concomitant surface marker downregulation upon in vitro culturing consistent with piecemeal degranulation. Lung eosinophils from mice with induced allergic airwa...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3758995</comments>
            <pubDate>Sun, 11 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3758995</guid>        </item>
        <item>
            <title>The TLR7 agonists imiquimod and gardiquimod improve DC-based immunotherapy for melanoma in mice.</title>
            <link>http://www.medworm.com/index.php?rid=3673031&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20543857%26dopt%3DAbstract</link>
            <description>In this study, we demonstrate that both gardiquimod and imiquimod promote the proliferation of murine splenocytes, stimulate the activation of splenic T, NK and natural killer T (NKT) cells, increase the cytolytic activity of splenocytes against B16 and MCA-38 tumor cell lines, and enhance the expression of costimulatory molecules and IL-12 by macrophages and bone marrow-derived dendritic cells (DCs). In a murine model, both agonists improved the antitumor effects of tumor lysate-loaded DCs, resulting in delayed growth of subcutaneous B16 melanoma tumors and suppression of pulmonary metastasis. Further, we found that gardiquimod demonstrated more potent antitumor activity than imiquimod. These results suggest that TLR7/8 agonists may serve as potent innate and adaptive immune response modi...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3673031</comments>
            <pubDate>Sun, 13 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3673031</guid>        </item>
        <item>
            <title>IL-17 signaling in host defense and inflammatory diseases.</title>
            <link>http://www.medworm.com/index.php?rid=3626206&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20514051%26dopt%3DAbstract</link>
            <description>Authors: Qian Y, Kang Z, Liu C, Li X
    Interleukin (IL)-17, the signature cytokine secreted by T helper (Th) 17 cells, plays important roles in host defense against extracellular bacterial infection and fungal infection and contributes to the pathogenesis of various autoimmune inflammatory diseases. Here we review the recent advances in IL-17-mediated functions with emphasis on the studies of IL-17-mediated signal transduction, providing perspective on potential drug targets for the treatment of autoimmune inflammatory diseases.Cellular &amp; Molecular Immunology advance online publication, 31 May 2010; doi:10.1038/cmi.2010.27.
    PMID: 20514051 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3626206</comments>
            <pubDate>Sun, 30 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3626206</guid>        </item>
        <item>
            <title>Programmed death-1 upregulation is correlated with dysfunction of tumor-infiltrating CD8(+) T lymphocytes in human non-small cell lung cancer.</title>
            <link>http://www.medworm.com/index.php?rid=3626205&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20514052%26dopt%3DAbstract</link>
            <description>In this study, we detected PD-1 expression on CD8(+) T cells from healthy control peripheral blood mononuclear cells (PBMCs) and the PBMCs of NSCLC patients as well as NSCLC tissues. Results showed that tumor-infiltrating CD8(+) T cells had increased PD-1 expression and impaired immune function, including reducing cytokine production capability and impairing capacity to proliferate. Blockade of the PD-1/PD-L1 pathway by the PD-L1-specific antibody partially restored cytokine production and cell proliferation. These data provide direct evidence that the PD-1/PD-L1 pathway is involved in CD8(+) T-cell dysfunction in NSCLC patients. Moreover, blocking this pathway provides a potential therapy target in lung cancer.Cellular &amp; Molecular Immunology advance online publication, 31 May 2010; do...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3626205</comments>
            <pubDate>Sun, 30 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3626205</guid>        </item>
        <item>
            <title>Arsenic trioxide alleviates airway hyperresponsiveness and eosinophilia in a murine model of asthma.</title>
            <link>http://www.medworm.com/index.php?rid=3596730&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20495578%26dopt%3DAbstract</link>
            <description>Authors: Chu KH, Lee CC, Hsin SC, Cai BC, Wang JH, Chiang BL
    Asthma is one of the most common chronic airway inflammatory diseases. The clinical hallmarks of asthma include elevated serum levels of immunoglobulin E (IgE), eosinophilic inflammation and airway hyper-responsiveness (AHR). Arsenic trioxide (As(2)O(3)) is considered a carcinogen; however, it has also been used to treat diseases, such as syphilis, in traditional Chinese and Western medicine. Today, As(2)O(3) is used as one of the standard therapies for acute promyelocytic leukemia (APL). Previous studies have indicated that As(2)O(3) can induce apoptosis in eosinophils. However, the effect of As(2)O(3) on asthma has not been investigated. We used ovalbumin (OVA)-immunized mice as a model for asthma and treated mice with As(2...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3596730</comments>
            <pubDate>Sun, 23 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3596730</guid>        </item>
        <item>
            <title>Distinct regulatory mechanism of immunoglobulin gene transcription in epithelial cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=3579130&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20473321%26dopt%3DAbstract</link>
            <description>Authors: Zhu X, Wu L, Zhang L, Hao P, Zhang S, Huang J, Zheng J, Liu Y, Li W, Zhang Y, Zhou C, Zhang Y, Yin C, Qiu X
    The restriction of immunoglobulin (Ig) expression to B lymphocytes is well established. However, several reports have confirmed that the Ig gene can be expressed in many non-B cancer cells and/or some normal cells. Our aim is to determine whether the Ig gene promoter can be activated in non-B cancer cells and to identify the regulatory mechanism for Ig gene expression. Our results show that the Ig promoter of VH4-59 was activated in several non-B cancer cell lines. Moreover, two novel positive regulatory elements, an enhancer-like element at -800 to -610 bp and a copromoter-like element at -610 to -300 bp, were identified in two epithelial cancer cell lines, HeLa S3 and ...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3579130</comments>
            <pubDate>Sun, 16 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3579130</guid>        </item>
        <item>
            <title>Cellular response to influenza virus infection: a potential role for autophagy in CXCL10 and interferon-alpha induction.</title>
            <link>http://www.medworm.com/index.php?rid=3579129&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20473322%26dopt%3DAbstract</link>
            <description>Authors: Law AH, Lee DC, Yuen KY, Peiris M, Lau AS
    Historically, influenza pandemics have arisen from avian influenza viruses. Avian influenza viruses H5N1 and H9N2 are potential pandemic candidates. Infection of humans with the highly pathogenic avian influenza H5N1 virus is associated with a mortality in excess of 60%, which has been attributed to dysregulation of the cytokine system. Human macrophages and epithelial cells infected with some genotypes of H5N1 and H9N2 viruses express markedly elevated cytokine and chemokine levels when compared with seasonal influenza A subtype H1N1 virus. The mechanisms underlying this cytokine and chemokine hyperinduction are not fully elucidated. In the present study, we demonstrate that autophagy, a tightly regulated homeostatic process for self-...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3579129</comments>
            <pubDate>Sun, 16 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3579129</guid>        </item>
        <item>
            <title>A Salmonella enterica serovar Typhi plasmid induces rapid and massive apoptosis in infected macrophages.</title>
            <link>http://www.medworm.com/index.php?rid=3579128&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20473323%26dopt%3DAbstract</link>
            <description>Authors: Wu S, Li Y, Xu Y, Li Q, Chu Y, Huang R, Qin Z
    pR(ST98) is a chimeric plasmid isolated from Salmonella enterica serovar Typhi (S. typhi) that mediates the functions of drug resistance and virulence. Previously, we reported that Salmonella plasmid virulence (spv) genes were present in S. typhi. In our current study, we investigated whether plasmid pR(ST98) exhibits significant cytotoxicity in macrophages. pR(ST98) was transferred into the avirulent Salmonella enterica serovar Typhimurium (S. typhimurium) strain RIA to create the transconjugant pR(ST98)/RIA. The standard S. typhimurium virulent strain SR-11, which carries a 100-kb virulence plasmid, was used as a positive control. The bacterial strains were incubated with a murine macrophage-like cell line (J774A.1) in vitro. Apo...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3579128</comments>
            <pubDate>Sun, 16 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3579128</guid>        </item>
        <item>
            <title>Functional characterization of the NF-kappaB binding site in the human NOD2 promoter.</title>
            <link>http://www.medworm.com/index.php?rid=3530684&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20436512%26dopt%3DAbstract</link>
            <description>Authors: Hu C, Sun L, Hu Y, Lu D, Wang H, Tang S
    Nucleotide-binding and oligomerization domain 2 (NOD2), a member of the NOD protein family, plays an important role in innate immunity. In response to pathogen attack, NOD2 stimulates cytokine and defensin production by activating nuclear factor (NF)-kappaB, a key transcription factor responsible for mediating downstream reactions. However, the mechanism linking NOD2 regulation and NF-kappaB activation is poorly understood. Using bioinformatics, we found a completely preserved canonical NF-kappaB binding site in the NOD2 core promoter (-16 to -25 bp) in both humans and chimpanzees. The functional role of this NF-kappaB binding site was investigated using the enhanced green fluorescent protein (EGFP) reporter system, site-directed mutagen...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3530684</comments>
            <pubDate>Sun, 02 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3530684</guid>        </item>
        <item>
            <title>Adenovirus-mediated LIGHT gene modification in murine B-cell lymphoma elicits a potent antitumor effect.</title>
            <link>http://www.medworm.com/index.php?rid=3507547&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20418899%26dopt%3DAbstract</link>
            <description>Authors: Hu G, Liu Y, Li H, Zhao D, Yang L, Shen J, Hong X, Cao X, Wang Q
    Here, we investigated the antitumor effect of adenovirus-mediated gene transfer of LIGHT, the tumor-necrosis factor (TNF) superfamily member also known as TNFSF14, in the murine A20 B-cell lymphoma. LIGHT gene modification resulted in upregulated expression of Fas and the accessory molecule-intercellular adhesion molecule-1 (ICAM-1) on A20 cells and led to enhanced A20 cell apoptosis. LIGHT-modified A20 cells effectively stimulated the proliferation of T lymphocytes and interferon (IFN)-gamma production in vitro. Immunization of BALB/c mice with a LIGHT-modified A20 cell vaccine efficiently elicited protective immunity against challenge with the parental tumor cell line. Adenovirus-mediated gene transfer of LIGHT...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3507547</comments>
            <pubDate>Sun, 25 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3507547</guid>        </item>
        <item>
            <title>Understanding the development and function of T follicular helper cells.</title>
            <link>http://www.medworm.com/index.php?rid=3464986&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20383172%26dopt%3DAbstract</link>
            <description>Authors: Nurieva RI, Chung Y
    A fundamental function of T helper (Th) cells is to regulate B-cell proliferation and immunoglobulin class switching, especially in the germinal centers. Th1 and Th2 lineages of CD4(+) T cells have long been considered to play an essential role in helping B cells by promoting the production immunoglobulin G2a (IgG2a) and IgG1/IgE, respectively. Recently, it has become clear that a subset CD4(+) T cells, named T follicular helper (Tfh) cells, is critical to B-cell response induction. In this review, we summarize the latest advances in our understanding of the regulation of Tfh cell differentiation, the relationship of Tfh cells to other CD4(+) T-cell lineages, and the role of Tfh cells in health and disease.Cellular &amp; Molecular Immunology advance online ...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3464986</comments>
            <pubDate>Sun, 11 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3464986</guid>        </item>
        <item>
            <title>Interleukin-17 and its expanding biological functions.</title>
            <link>http://www.medworm.com/index.php?rid=3464985&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20383173%26dopt%3DAbstract</link>
            <description>Authors: Xu S, Cao X
    Interleukin-17 (IL-17) and IL-17-producing cells have been shown to play important roles in inflammation and the immune response. IL-17 is believed to be mainly produced by T helper 17 (Th17) cells, a unique helper T-cell subset different from Th1 and Th2 cells. Other subsets of T cells such as gammadeltaT and natural killer T (NKT) cells have also been found to produce IL-17 in response to innate stimuli. IL-17 acts as a proinflammatory cytokine that can induce the release of certain chemokines, cytokines, matrix metalloproteinases (MMPs) and antimicrobial peptides from mesenchymal and myeloid cells. This leads to the expansion and accumulation of neutrophils in the innate immune system and links innate and adaptive immunity in vivo. Furthermore, increasing eviden...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3464985</comments>
            <pubDate>Sun, 11 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3464985</guid>        </item>
        <item>
            <title>The cytokine milieu in the interplay of pathogenic Th1/Th17 cells and regulatory T cells in autoimmune disease.</title>
            <link>http://www.medworm.com/index.php?rid=3464984&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20383174%26dopt%3DAbstract</link>
            <description>The objective of an effective therapeutic approach for autoimmune disease is to restore this balance. In this review, we describe the characteristics and development of pathogenic T helper 1 (Th1) and Th17 cells and the beneficial Treg cells in autoimmune diseases and the crucial roles of the cytokine milieu in influencing the balance of these T-cell subsets. Given the importance of cytokines, we discuss current immunotherapeutic strategies using cytokine or cytokine receptor antibodies for the treatment of autoimmune diseases. Cellular &amp; Molecular Immunology advance online publication, 19 April 2010; doi:10.1038/cmi.2010.22.
    PMID: 20383174 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3464984</comments>
            <pubDate>Sun, 11 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3464984</guid>        </item>
        <item>
            <title>Regulatory T cells: immune suppression and beyond.</title>
            <link>http://www.medworm.com/index.php?rid=3464983&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20383175%26dopt%3DAbstract</link>
            <description>Authors: Wan YY
    Foxp3-expressing regulatory T cells (Tregs) were originally identified as critical in maintaining self-tolerance and immune homeostasis. The immunosuppressive functions of Tregs are widely acknowledged and have been extensively studied. Recent studies have revealed many diverse roles of Tregs in shaping the immune system and the inflammatory response. This review will discuss our efforts as well as the efforts of others towards understanding the multifaceted function of Tregs in immune regulation. Cellular &amp; Molecular Immunology advance online publication, 19 April 2010; doi:10.1038/cmi.2010.20.
    PMID: 20383175 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3464983</comments>
            <pubDate>Sun, 11 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3464983</guid>        </item>
        <item>
            <title>Receptor-interacting protein (RIP) kinase family.</title>
            <link>http://www.medworm.com/index.php?rid=3464982&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20383176%26dopt%3DAbstract</link>
            <description>Authors: Zhang D, Lin J, Han J
    Receptor-interacting protein (RIP) kinases are a group of threonine/serine protein kinases with a relatively conserved kinase domain but distinct non-kinase regions. A number of different domain structures, such as death and caspase activation and recruitment domain (CARD) domains, were found in different RIP family members, and these domains should be keys in determining the specific function of each RIP kinase. It is known that RIP kinases participate in different biological processes, including those in innate immunity, but their downstream substrates are largely unknown. This review will give an overview of the structures and functions of RIP family members, and an update of recent progress in RIP kinase research.Cellular &amp; Molecular Immunology ad...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3464982</comments>
            <pubDate>Sun, 11 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3464982</guid>        </item>
        <item>
            <title>Bisphenol A in combination with TNF-alpha selectively induces Th2 cell-promoting dendritic cells in vitro with an estrogen-like activity.</title>
            <link>http://www.medworm.com/index.php?rid=3464974&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20383177%26dopt%3DAbstract</link>
            <description>Authors: Guo H, Liu T, Uemura Y, Jiao S, Wang D, Lin Z, Narita Y, Suzuki M, Hirosawa N, Ichihara Y, Ishihara O, Kikuchi H, Sakamoto Y, Senju S, Zhang Q, Ling F
    Bisphenol A (BPA) is a monomer used in manufacturing a wide range of chemical products, including epoxy resins and polycarbonate. BPA, an important endocrine disrupting chemical that exerts estrogen-like activities, is detectable at nanomolar levels in human serum worldwide. The pregnancy associated doses of 17beta-estradiol (E2) plus tumor-necrosis factor-alpha (TNF-alpha) induce distorted maturation of human dendritic cells (DCs) that result in an increased capacity to induce T helper (Th) 2 responses. The current study demonstrated that the presence of BPA during DC maturation influences the function of human DCs, thereby pol...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3464974</comments>
            <pubDate>Sun, 11 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3464974</guid>        </item>
        <item>
            <title>HDAC4 inhibits the transcriptional activation of mda-7/IL-24 induced by Sp1.</title>
            <link>http://www.medworm.com/index.php?rid=3464967&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20383178%26dopt%3DAbstract</link>
            <description>In this study, we show that the expression of mda-7/IL-24 was upregulated by the histone deacetylase (HDAC) inhibitors trichostatin A (TSA) and sodium butyrate (NaBu), whereas it was downregulated by HDAC4. We also found that the histone acetylation level and the binding of the transcriptional factor Sp1 to the mad-7 promoter were reduced upon HDAC4 treatment. Moreover, the HDAC inhibitor TSA induced histone hyperacetylation and stimulated Sp1 binding to the mda-7/IL-24 promoter, which in turn enhanced the expression of mda-7/IL-24. Therefore, we conclude that histone acetylation modification plays an important role in the regulation of mda-7/IL-24 and that the transcription factor Sp1 participates in this process.Cellular &amp; Molecular Immunology advance online publication, 12 April 201...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3464967</comments>
            <pubDate>Sun, 11 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3464967</guid>        </item>
        <item>
            <title>microRNAs: critical regulators in Th17 cells and players in diseases.</title>
            <link>http://www.medworm.com/index.php?rid=3449677&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20364159%26dopt%3DAbstract</link>
            <description>Authors: Wei B, Pei G
    microRNAs are a novel group of small, conserved, non-coding RNA molecules that are present in all species. These molecules post-transcriptionally regulate gene expression by targeting mRNAs for degradation or by repressing the translation of the mRNAs. A good understanding of miRNA-mediated gene regulation is critical to gain a comprehensive view of many physiological processes and disease states. Emerging evidence demonstrates that miRNAs play an important role in the differentiation and function of the adaptive immune system. This review provides an overview of the diverse functions of miRNAs in modulating immune responses and in immune cell development, particularly the development of Th17 cells, and explores the involvement of miRNAs in several autoimmune dise...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3449677</comments>
            <pubDate>Sun, 04 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3449677</guid>        </item>
        <item>
            <title>Multiple checkpoints keep follicular helper T cells under control to prevent autoimmunity.</title>
            <link>http://www.medworm.com/index.php?rid=3449676&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20364160%26dopt%3DAbstract</link>
            <description>Authors: Yu D, Vinuesa CG
    Follicular helper T (Tfh) cells select mutated B cells in germinal centres, which can then differentiate into long-lived high affinity memory B cells and plasma cells. Tfh cells are regulated by a unique molecular programme orchestrated by the transcriptional repressor Bcl6. This transcription factor turns down expression of multiple genes, including transcriptional regulators of other T helper lineages and a vast amount of microRNAs. This enables Tfh cells to express a suite of chemokine receptors, stimulatory ligands and cytokines that enable migration into B-cell follicles, and provision of effective help to B cells. Not surprisingly, dysregulation of this powerful helper subset can lead to a range of autoantibody-mediated diseases; indeed, aberrant accumul...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3449676</comments>
            <pubDate>Sun, 04 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3449676</guid>        </item>
        <item>
            <title>Curcumin reverses T cell-mediated adaptive immune dysfunctions in tumor-bearing hosts.</title>
            <link>http://www.medworm.com/index.php?rid=3399578&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20305684%26dopt%3DAbstract</link>
            <description>Authors: Bhattacharyya S, Md Sakib Hossain D, Mohanty S, Sankar Sen G, Chattopadhyay S, Banerjee S, Chakraborty J, Das K, Sarkar D, Das T, Sa G
    Immune dysfunction is well documented during tumor progression and likely contributes to tumor immune evasion. CD8(+) cytotoxic T lymphocytes (CTLs) are involved in antigen-specific tumor destruction and CD4(+) T cells are essential for helping this CD8(+) T cell-dependent tumor eradication. Tumors often target and inhibit T-cell function to escape from immune surveillance. This dysfunction includes loss of effector and memory T cells, bias towards type 2 cytokines and expansion of T regulatory (Treg) cells. Curcumin has previously been shown to have antitumor activity and some research has addressed the immunoprotective potential of this plant...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3399578</comments>
            <pubDate>Mon, 22 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3399578</guid>        </item>
        <item>
            <title>The enigmatic processing and secretion of interleukin-33.</title>
            <link>http://www.medworm.com/index.php?rid=3399577&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20305685%26dopt%3DAbstract</link>
            <description>Authors: Zhao W, Hu Z
    Interleukin-33 (IL-33) is the most attractive novel cytokine identified as an IL-1 family member. IL-33 was first named NF-HEV (nuclear factor from high endothelial venules), as it was known to interact with nuclear chromatin although its exact intracellular functions are still to be clarified. IL-33 is now recognized as the specific ligand for the orphan IL-1 receptor family member ST2 and to be involved in polarization of T cells towards T helper 2 cell phenotype and in activation of mast cells, bosophils, eosinophils and natural killer cells. It is essential for IL-33 to be extracellularly released in order to bind to the ST2 receptor and consequently play a crucial role in inflammatory, infectious and autoimmune diseases. However, like the IL-1 family members,...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3399577</comments>
            <pubDate>Mon, 22 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3399577</guid>        </item>
        <item>
            <title>Th17 cells and their associated cytokines in liver diseases.</title>
            <link>http://www.medworm.com/index.php?rid=3399576&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20305686%26dopt%3DAbstract</link>
            <description>Authors: Lafdil F, Miller AM, Ki SH, Gao B
    T helper 17 (Th17) cells are a newly identified subset of T helper cells that play important roles in host defense against extracellular bacteria as well as in the pathogenesis of autoimmune disease. The functions of Th17 cells are mediated via the production of several cytokines including interleukin (IL)-17 and IL-22. Recent studies show that the frequency of IL-17(+) cells is significantly elevated in a variety of chronic liver diseases including alcoholic liver disease, viral hepatitis and hepatocellular carcinoma. IL-17 receptor is expressed virtually on all types of liver cells, while IL-22 receptor expression is restricted to epithelial cells including hepatocytes in the liver. IL-17 seems to play an important role in inducing liver inf...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3399576</comments>
            <pubDate>Mon, 22 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3399576</guid>        </item>
        <item>
            <title>Th1 cytokines promote T-cell binding to antigen-presenting cells via enhanced hyaluronan production and accumulation at the immune synapse.</title>
            <link>http://www.medworm.com/index.php?rid=3371096&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20228832%26dopt%3DAbstract</link>
            <description>Authors: Bollyky PL, Evanko SP, Wu RP, Potter-Perigo S, Long SA, Kinsella B, Reijonen H, Guebtner K, Teng B, Chan CK, Braun KR, Gebe JA, Nepom GT, Wight TN
    Hyaluronan (HA) production by dendritic cells (DCs) is known to promote antigen presentation and to augment T-cell activation and proliferation. We hypothesized that pericellular HA can function as intercellular 'glue' directly mediating T cell-DC binding. Using primary human cells, we observed HA-dependent binding between T cells and DCs, which was abrogated upon pre-treatment of the DCs with 4-methylumbelliferone (4-MU), an agent which blocks HA synthesis. Furthermore, T cells regulate HA production by DCs via T cell-derived cytokines in a T helper (Th) subset-specific manner, as demonstrated by the observation that cell-culture s...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3371096</comments>
            <pubDate>Mon, 15 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3371096</guid>        </item>
        <item>
            <title>Effects of NS1 variants of H5N1 influenza virus on interferon induction, TNFalpha response and p53 activity.</title>
            <link>http://www.medworm.com/index.php?rid=3371095&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20228833%26dopt%3DAbstract</link>
            <description>We examined the effects of these mutations on interferon (IFN) induction, tumor-necrosis factor (TNF)alpha response, p53 activity and apoptosis. We found that the D92E mutation eliminated NS1's repressive effect on IFN induction, while the 5-aa deletion resulted in enhanced resistance to TNFalpha responses. We also observed that all three variants exhibited a similar suppressive effect on p53 transcriptional activity, although none of them significantly influenced apoptosis of host cells. Our findings shed new light on the role of NS1 in the pathogenicity of H5N1 virus.Cellular &amp; Molecular Immunology advance online publication, 15 March 2010; doi:10.1038/cmi.2010.6.
    PMID: 20228833 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3371095</comments>
            <pubDate>Mon, 15 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3371095</guid>        </item>
        <item>
            <title>The good and evil of complement activation in HIV-1 infection.</title>
            <link>http://www.medworm.com/index.php?rid=3371094&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20228834%26dopt%3DAbstract</link>
            <description>Authors: Yu Q, Yu R, Qin X
    The complement system, a key component of innate immunity, is a first-line defender against foreign pathogens such as HIV-1. The role of the complement system in HIV-1 pathogenesis appears to be multifaceted. Although the complement system plays critical roles in clearing and neutralizing HIV-1 virions, it also represents a critical factor for the spread and maintenance of the virus in the infected host. In addition, complement regulators such as human CD59 present in the envelope of HIV-1 prevent complement-mediated lysis of HIV-1. Some novel approaches are proposed to combat HIV-1 infection through the enhancement of antibody-dependent complement activity against HIV-1. In this paper, we will review these diverse roles of complement in HIV-1 infection.Cellu...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3371094</comments>
            <pubDate>Mon, 15 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3371094</guid>        </item>
        <item>
            <title>An isoleucine-zipper motif enhances costimulation of human soluble trimeric GITR ligand.</title>
            <link>http://www.medworm.com/index.php?rid=3371093&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20228835%26dopt%3DAbstract</link>
            <description>In conclusion, the incorporation of an ILZ motif could markedly improve the costimulation of hsGITRL.Cellular &amp; Molecular Immunology advance online publication, 15 March 2010; doi:10.1038/cmi.2010.7.
    PMID: 20228835 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3371093</comments>
            <pubDate>Mon, 15 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3371093</guid>        </item>
        <item>
            <title>Photodynamic therapy-mediated modulation of inflammatory cytokine production by Epstein-Barr virus-infected nasopharyngeal carcinoma cells.</title>
            <link>http://www.medworm.com/index.php?rid=3371092&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20228836%26dopt%3DAbstract</link>
            <description>This study aims to examine the effects of EBV infection on the production of proinflammatory cytokines in NPC cells after the Zn-BC-AM photodynamic therapy (PDT) treatment. Cells were treated with the photosensitiser Zn-BC-AM for 24 h before light irradiation. Quantitative ELISA was used to evaluate the production of cytokines. Under the same experimental condition, HK-1-EBV cells produced a higher basal level of IL-1alpha (1561 pg/ml), IL-1beta (16.6 pg/ml) and IL-8 (422.9 pg/ml) than the HK-1 cells. At the light dose of 0.25-0.5 J/cm(2), Zn-BC-AM PDT-treated HK-1-EBV cells were found to produce a higher level of IL-1alpha and IL-1beta than the HK-1 cells. The production of IL-1beta appeared to be mediated via the IL-1beta-converting enzyme (ICE)-independent pathway. In contrast, the prod...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3371092</comments>
            <pubDate>Mon, 15 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3371092</guid>        </item>
        <item>
            <title>Interplay between Helicobacter pylori and immune cells in immune pathogenesis of gastric inflammation and mucosal pathology.</title>
            <link>http://www.medworm.com/index.php?rid=3319064&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20190789%26dopt%3DAbstract</link>
            <description>This article will review the recent novel findings on the interactions of H. pylori with diverse host epithelial signaling pathways and events involved in the initiation of gastric pathology, including gastric inflammation, mucosal damage and development of MALT lymphomas.
    PMID: 20190789 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3319064</comments>
            <pubDate>Mon, 01 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3319064</guid>        </item>
        <item>
            <title>The complicated role of NF-kappaB in T-cell selection.</title>
            <link>http://www.medworm.com/index.php?rid=3319063&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20190822%26dopt%3DAbstract</link>
            <description>Authors: Zhu M, Fu Y
    The nuclear factor (NF)-kappaB transcription factor family plays important roles in the immune system. Aberrant NF-kappaB signaling is frequently associated with inflammation and autoimmune diseases but the underlying mechanisms are not fully understood. Recent studies show that NF-kappaB plays a critical role in T-cell central tolerance. Two NF-kappaB signaling pathways have been identified: the canonical pathway and the alternative pathway. In the establishment of T-cell central tolerance, the alternative pathway appears to be the key signaling component in thymic stromal cells for their development and function, while the canonical pathway exerts its function more in autonomous T-cell selection. This review intends to summarize the current understanding of the r...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3319063</comments>
            <pubDate>Mon, 01 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3319063</guid>        </item>
        <item>
            <title>CD24: from A to Z.</title>
            <link>http://www.medworm.com/index.php?rid=3276803&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20154703%26dopt%3DAbstract</link>
            <description>Authors: Fang X, Zheng P, Tang J, Liu Y
    As a testament to the importance of CD24, researchers with diverse interests, including adaptive immunity, inflammation, autoimmune diseases and cancer, have encountered CD24. CD24 is overexpressed in many cancers and appears oncogenic. In the adaptive immune response, CD24 is a redundant costimulatory molecule in costimulation-rich lymphoid organs but is essential in selected target organs tested, such as brain and skin. More recent studies suggest it may have a role in discriminating danger and pathogen-associated molecular patterns by dendritic cells. The biology of CD24 is intriguing but poorly understood. Here we summarize the major findings associated with CD24 to stimulate new ideas for further research that may reveal the underlying link ...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3276803</comments>
            <pubDate>Mon, 15 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3276803</guid>        </item>
        <item>
            <title>Blockade of CD28 by a synthetical peptoid inhibits T-cell proliferation and attenuates graft-versus-host disease.</title>
            <link>http://www.medworm.com/index.php?rid=3255093&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20140006%26dopt%3DAbstract</link>
            <description>Authors: Li N, Zhu F, Gao F, Wang Q, Wang X, Li H, Ma C, Sun W, Xu W, Wang C, Zhang L
    CD28 is one of the costimulatory molecules crucial for T-cell activation and thus has become an attractive target for therapeutic immunomodulation. Conventional strategies for blocking CD28 activity using monoclonal antibodies, Fab fragments, antagonistic peptide and fusion proteins, have apparent disadvantages such as inherent immunogenicity, unwanted Fc signaling, poor tissue penetration and bioinstability. Recent research has been directed toward the creation of non-natural, sequence-specific biomimetic oligomers with bioinspired structures that capture the amino-acid interface of the targeted proteins. One such family of molecules is the poly-N-substituted glycines or peptoids, which have close st...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3255093</comments>
            <pubDate>Mon, 08 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3255093</guid>        </item>
        <item>
            <title>Epigallocatechin-3-gallate (EGCG) attenuates inflammation in MRL/lpr mouse mesangial cells.</title>
            <link>http://www.medworm.com/index.php?rid=3255092&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20140007%26dopt%3DAbstract</link>
            <description>Authors: Peairs A, Dai R, Gan L, Shimp S, Rylander MN, Li L, Reilly CM
    Epigallocatechin-3-gallate (EGCG), a bioactive component of green tea, has been reported to exert anti-inflammatory effects on immune cells. EGCG is also shown to activate the metabolic regulator, adenosine 5'-monophosphate-activated protein kinase (AMPK). Reports have also indicated that EGCG inhibits the immune-stimulated phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway. The PI3K/Akt/mTOR pathway has been implicated in mesangial cell activation in lupus. Mesangial cells from MRL/lpr lupus-like mice are hyper-responsive to immune stimulation and overproduce nitric oxide (NO) and other inflammatory mediators when stimulated. In our current studies, we sought to determine the mechanis...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3255092</comments>
            <pubDate>Mon, 08 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3255092</guid>        </item>
        <item>
            <title>Role of activating transcription factor 3 (ATF3) in sublytic C5b-9-induced glomerular mesangial cell apoptosis.</title>
            <link>http://www.medworm.com/index.php?rid=3255091&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20140008%26dopt%3DAbstract</link>
            <description>In this study, ATF3 expression and cell apoptosis in GMCs induced by sublytic C5b-9 were measured, and then the effects of ATF3 gene over-expression or knockdown on GMC apoptosis induced by sublytic C5b-9 were examined at a fixed time. The results showed that both ATF3 expression and GMC apoptosis were markedly increased and ATF3 over-expression obviously increased sublytic C5b-9-induced GMC apoptosis, whereas ATF3 gene silencing had a significant opposite effect. Collectively, these findings indicate that upregulation of ATF3 gene expression is involved in regulating GMC apoptosis induced by sublytic C5b-9 complexes.
    PMID: 20140008 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3255091</comments>
            <pubDate>Mon, 08 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3255091</guid>        </item>
        <item>
            <title>Premetastatic milieu explained by TLR4 agonist-mediated homeostatic inflammation.</title>
            <link>http://www.medworm.com/index.php?rid=3255090&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20140009%26dopt%3DAbstract</link>
            <description>Authors: Maru Y
    Accumulating evidence suggests that Toll-like receptor 4 (TLR4), a sensor for danger signals, is expressed not only in immune cells, but also in resident epithelial cells, and appears to participate in tissue homeostasis. To explain the premetastatic microenvironment created by the newly discovered endogenous TLR4 ligands, I propose a hypothesis of homeostatic inflammation that includes the classical danger hypothesis.
    PMID: 20140009 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3255090</comments>
            <pubDate>Mon, 08 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3255090</guid>        </item>
        <item>
            <title>Enhancement of antitumor immunity by low-dose total body irradiation is associated with selectively decreasing the proportion and number of T regulatory cells.</title>
            <link>http://www.medworm.com/index.php?rid=3255089&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20140010%26dopt%3DAbstract</link>
            <description>In this study, by analyzing the immune patterns of lymphocytes, we found that the percentage and absolute number of CD4(+)CD25(+)Foxp3(+) regulatory T cells are markedly decreased in naive mice following treatment with LTBI. On the contrary, the CD4(+)CD44(+)/CD8(+)CD44(+) effector-memory T cells are greatly increased. Importantly, naive mice treated with dendritic cell-gp100 tumor vaccines under LTBI induced an enhancement of antigen-specific proliferation and cytotoxicity as well as interferon-gamma (IFN-gamma) secretion against F10 melanoma tumor challenge, compared to treatment with either the tumor vaccine or LTBI alone. Consequently, the treatment resulted in a reduced tumor burden and prolonged mouse survival. Our data demonstrate that LTBI's enhancement of antitumor immunity was ma...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3255089</comments>
            <pubDate>Mon, 08 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3255089</guid>        </item>
        <item>
            <title>Increased expression of human T-cell immunoglobulin- and mucin-domain-containing molecule-4 in peripheral blood mononuclear cells from patients with system lupus erythematosus.</title>
            <link>http://www.medworm.com/index.php?rid=3255088&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20140011%26dopt%3DAbstract</link>
            <description>In this study, we used quantitative real-time reverse transcription-polymerase chain reaction to examine the mRNA expression of Tim-4 in peripheral blood mononuclear cells (PBMCs) from SLE patients and further analyzed the correlation between the expression of Tim-4 and Tim-1 (a potential ligand for Tim-4) in PBMCs and serum tumor necrosis factor (TNF)-alpha levels. The results showed that Tim-4 mRNA expression in PBMCs was significantly higher in SLE patients than in healthy controls, especially those patients in the active phase of disease. Moreover, Tim-4 mRNA levels were closely correlated with Tim-1 mRNA levels in PBMCs and with serum TNF-alpha levels in SLE patients but not in the control group. Taken together, these results demonstrate that Tim-4 may be involved in the pathogenesis ...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3255088</comments>
            <pubDate>Mon, 08 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3255088</guid>        </item>
        <item>
            <title>Response of BALB/c mice to a monovalent influenza A (H1N1) 2009 split vaccine.</title>
            <link>http://www.medworm.com/index.php?rid=3228279&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20118968%26dopt%3DAbstract</link>
            <description>In conclusion, the present study provides support for the clinical evaluation of influenza A (H1N1) vaccination as a public health intervention to mitigate a possible pandemic. Additionally, our findings support the further evaluation of the vaccine used in this study in primates or humans.
    PMID: 20118968 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3228279</comments>
            <pubDate>Mon, 01 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3228279</guid>        </item>
        <item>
            <title>Roles of autophagy in lymphocytes: reflections and directions.</title>
            <link>http://www.medworm.com/index.php?rid=3228278&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20118969%26dopt%3DAbstract</link>
            <description>Authors: McLeod IX, He Y
    Recent studies have revealed that autophagy, a fundamental intracellular process, plays many different roles in lymphocyte development and function. Autophagy regulates naive T-lymphocyte homeostasis, specifically by regulating mitochondrial quality and turnover, and is necessary for the proliferation of mature T cells. Autophagy also acts as a cellular death pathway in lymphocytes, both upon prolonged cytokine withdrawal and during acute antigen-receptor stimulation if improperly regulated. Furthermore, during HIV infection, hyperinduction of autophagy leads to massive T-cell death in uninfected CD4(+) T cells, and is rescued by inhibiting autophagic initiation. Constitutively high levels of autophagy in thymic epithelial cells are necessary for optimal proces...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3228278</comments>
            <pubDate>Mon, 01 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3228278</guid>        </item>
        <item>
            <title>Regeneration of dendritic cells in aged mice.</title>
            <link>http://www.medworm.com/index.php?rid=3228277&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20118970%26dopt%3DAbstract</link>
            <description>Authors: van Dommelen SL, Rizzitelli A, Chidgey A, Boyd R, Shortman K, Wu L
    Age-related thymic involution causes a decreased output of thymocytes from the thymus, thereby resulting in impairment of T cell-mediated immunity. While alterations in the T cell and non-haematopoietic stromal compartments have been described, the effects of thymic involution on thymic dendritic cells (DC) are not clearly known. Thymic DC play an essential role in shaping T cell-mediated immune responses by deleting self-reactive thymocytes to establish central tolerance and by inducing regulatory T-cell (Treg) development. It is therefore important to assess the prevalence of and alterations to thymic DC with age, as this may impact on their function. We assessed the numbers and proportions of the three disti...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3228277</comments>
            <pubDate>Mon, 01 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3228277</guid>        </item>
        <item>
            <title>Regulation of immune cell responses by semaphorins and their receptors.</title>
            <link>http://www.medworm.com/index.php?rid=3228276&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20118971%26dopt%3DAbstract</link>
            <description>Authors: Takamatsu H, Okuno T, Kumanogoh A
    Semaphorins were originally identified as axon guidance factors involved in the development of the neuronal system. However, accumulating evidence indicates that several members of semaphorins, so-called 'immune semaphorins', are crucially involved in various phases of immune responses. These semaphorins regulate both immune cell interactions and immune cell trafficking during physiological and pathological immune responses. Here, we review the following two functional aspects of semaphorins and their receptors in immune responses: their functions in cell-cell interactions and their involvement in immune cell trafficking.
    PMID: 20118971 [PubMed - as supplied by publisher] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3228276</comments>
            <pubDate>Mon, 01 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3228276</guid>        </item>
        <item>
            <title>A novel interface consisting of homologous immunoglobulin superfamily members with multiple functions.</title>
            <link>http://www.medworm.com/index.php?rid=3186275&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20081873%26dopt%3DAbstract</link>
            <description>Authors: Xu Z, Jin B
    Immunoglobulin superfamily (IgSF) members account for a large proportion of cell adhesion molecules that perform important immunological functions, including recognizing a variety of counterpart molecules on the cell surface or extracellular matrix. The findings that CD155/poliovirus receptor (PVR) and CD112/nectin-2 are the ligands for CD226/platelet and T-cell activation antigen 1 (PTA1)/DNAX accessory molecular-1 (DNAM-1), CD96/tactile and Washington University cell adhesion molecule (WUCAM) and that CD226 is physically and functionally associated with lymphocyte function-associated antigen-1 (LFA-1) on natural killer (NK) and activated T cells have largely expanded our knowledge about the functions of CD226, CD96, WUCAM and LFA-1 and their respective ligands, C...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3186275</comments>
            <pubDate>Fri, 01 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3186275</guid>        </item>
        <item>
            <title>TGF-beta1 gene-modified, immature dendritic cells delay the development of inflammatory bowel disease by inducing CD4(+)Foxp3(+) regulatory T cells.</title>
            <link>http://www.medworm.com/index.php?rid=3186274&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20081874%26dopt%3DAbstract</link>
            <description>In conclusion, we provide evidence that TGF-beta1-modified bone marrow-derived imDCs may have a therapeutic effect to IBD.
    PMID: 20081874 [PubMed - in process] (Source: Cellular and Molecular Immunology)</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3186274</comments>
            <pubDate>Fri, 01 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3186274</guid>        </item>
        <item>
            <title>CD40-activated B cells are more potent than immature dendritic cells to induce and expand CD4(+) regulatory T cells.</title>
            <link>http://www.medworm.com/index.php?rid=3186273&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20081875%26dopt%3DAbstract</link>
            <description>In this study, we found that CD40-B exhibited mature phenotypes and were more able to induce and expand CD4(high)CD25(+) Tregs than imDCs. Moreover, Tregs induced by CD40-B had greater suppressive capacity than those induced by imDCs. The generation of CD4(high)CD25(+) Tregs by CD40-B and imDCs is cell-cell contact dependent and partially relies on the expression of human leukocyte antigen (HLA)-DR and CD80/86. Differences in CD4(high)CD25(+) Treg generation efficiency were largely explained by the production of endogenous IL-2 by CD40-B. Our results suggest that CD40-B is better able to generate large numbers of antigen-specific Tregs than imDCs. Additionally, using CD40-B to generate Tregs may accelerate the clinical use of Treg-based immunotherapy in the treatment of allograft rejection...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3186273</comments>
            <pubDate>Fri, 01 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3186273</guid>        </item>
        <item>
            <title>Abnormal regulation of chemokine TECK and its receptor CCR9 in the endometriotic milieu is involved in pathogenesis of endometriosis by way of enhancing invasiveness of endometrial stromal cells.</title>
            <link>http://www.medworm.com/index.php?rid=3186272&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20081876%26dopt%3DAbstract</link>
            <description>Authors: Wang Y, Yu J, Luo X, Wang X, Li M, Wang L, Li D
    The chemokine thymus-expressed chemokine (TECK), which regulates T-cell development and tissue-specific homing, has been identified as a potential contributor to the pathogenesis and progression of endometriosis. Dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin, TCDD), an air pollutant, and estrogen also appear to be involved in endometriosis. Both endometrial stromal cells (ESCs) and the combination of 17beta-estradiol and TCDD increase the secretion of TECK in the endometriosis-associated cells and promote the invasiveness of ESCs by increasing expression of matrix metalloproteinase (MMP)-2 and MMP-9. Anti-TECK neutralizing antibodies can effectively inhibit the invasiveness of ESCs and the expression of MMP-2 and MMP-9 in the cells...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3186272</comments>
            <pubDate>Fri, 01 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3186272</guid>        </item>
        <item>
            <title>Modulation of morphological changes of microglia and neuroprotection by monocyte chemoattractant protein-1 in experimental glaucoma.</title>
            <link>http://www.medworm.com/index.php?rid=3186271&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20081877%26dopt%3DAbstract</link>
            <description>Authors: Chiu K, Yeung SC, So KF, Chang RC
    Monocyte chemoattractant protein-1 (MCP-1)/CCL2 is a C-C chemokine involved in the activation and recruitment of monocytic cells to injury sites. MCP-1/CCL2 can induce either neuroprotection or neurodestruction in vitro, depending on the experimental model. We aim to use MCP-1/CCL2 as an experimental tool to investigate the morphological changes of microglia when loss of healthy retinal ganglion cells (RGCs) is exacerbated or attenuated in an experimental glaucoma model. While a high concentration (1000 ng) of MCP-1/CCL2 and lipopolysaccharide (LPS)-exacerbated RGC loss, 100 ng MCP-1/CCL2 provided neuroprotection towards RGC. Neuroprotective MCP-1/CCL2 (100 ng) also upregulated insulin-like growth factor-1 (IGF-1) immunoreactivity in the RGCs....</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3186271</comments>
            <pubDate>Fri, 01 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3186271</guid>        </item>
        <item>
            <title>Hypoxia induces T-cell apoptosis by inhibiting chemokine C receptor 7 expression: the role of adenosine receptor A(2).</title>
            <link>http://www.medworm.com/index.php?rid=3119459&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20029460%26dopt%3DAbstract</link>
            <description>Authors: Sun J, Zhang Y, Yang M, Zhang Y, Xie Q, Li Z, Dong Z, Yang Y, Deng B, Feng A, Hu W, Mao H, Qu X
    Hypoxia is a major characteristic of the tumor microenvironment, and its effects on immune cells are proposed to be important factors for the process of tumor immune escape. It has been reported that hypoxia affects the function of dendritic cells and the antitumor function of T cells. Here we discuss the effects of hypoxia on T-cell survival. Our results showed that hypoxia induced apoptosis of T cells. Adenosine and adenosine receptors (AR) are important to the hypoxia-related signaling pathway. Using AR agonists and antagonists, we demonstrated that hypoxia-induced apoptosis of T cells was mediated by A(2a )and A(2b) receptors. Furthermore, we are the first, to our knowledge, to ...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3119459</comments>
            <pubDate>Wed, 23 Dec 2009 00:00:00 +0100</pubDate>
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            <title>Intracellular signaling mechanisms regulating the activation of human eosinophils by the novel Th2 cytokine IL-33: implications for allergic inflammation.</title>
            <link>http://www.medworm.com/index.php?rid=3119458&amp;cid=s_37766_67_f&amp;fid=37766&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20029461%26dopt%3DAbstract</link>
            <description>Authors: Chow JY, Wong CK, Cheung PF, Lam CW
    The novel interleukin (IL)-1 family cytokine IL-33 has been shown to activate T helper 2 (Th2) lymphocytes, mast cells and basophils to produce an array of proinflammatory cytokines, as well as to mediate blood eosinophilia, IgE secretion and hypertrophy of airway epithelium in mice. In the present study, we characterized the activation of human eosinophils by IL-33, and investigated the underlying intracellular signaling mechanisms. IL-33 markedly enhanced eosinophil survival and upregulated cell surface expression of the adhesion molecule intercellular adhesion molecule (ICAM)-1 on eosinophils, but it suppressed that of ICAM-3 and L-selectin. In addition, IL-33 mediates significant release of the proinflammatory cytokine IL-6 and the chemo...</description>
            <author>Cellular and Molecular Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3119458</comments>
            <pubDate>Wed, 23 Dec 2009 00:00:00 +0100</pubDate>
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