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        <title>Clinical 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 'Clinical Immunology' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Clinical+Immunology&t=Clinical+Immunology&s=Search&f=source]]></link>
        <lastBuildDate>Wed, 08 Feb 2012 06:42:48 +0100</lastBuildDate>
        <item>
            <title>Live Attenuated Influenza Virus (LAIV) induces different mucosal T cell function in nonsmokers and smokers.</title>
            <link>http://www.medworm.com/index.php?rid=5625215&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22264637%26dopt%3DAbstract</link>
            <description>Authors: Horvath KM, Brighton LE, Herbst M, Noah TL, Jaspers I
    Abstract
    Smokers are more susceptible to respiratory infections, including influenza. To explore the effect of smoking on influenza-induced responses within the nasal mucosa, we have developed a protocol using inoculation with live attenuated influenza virus (LAIV) vaccine followed by sampling of the nasal mucosa. Mucosal cell populations were harvested through superficial biopsy of the nasal inferior turbinate pre and post LAIV inoculation and analyzed using flow cytometry. The majority of nasal biopsy CD45+ immune cells at baseline were CD3+ T lymphocytes. Following LAIV, these lymphocytes increased in nonsmokers but not in smokers. A subset of individuals was negative for helper T cell marker CD4 and cytotoxic T cell...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5625215</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5625215</guid>        </item>
        <item>
            <title>Immune modulation by Lacto-N-fucopentaose III in experimental autoimmune encephalomyelitis.</title>
            <link>http://www.medworm.com/index.php?rid=5625216&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22264636%26dopt%3DAbstract</link>
            <description>Authors: Zhu B, Trikudanathan S, Zozulya AL, Sandoval-Garcia C, Kennedy JK, Atochina O, Norberg T, Castagner B, Seeberger P, Fabry Z, Harn D, Khoury SJ, Guleria I
    Abstract
    Parasitic infections frequently lead to immune deviation or suppression. However, the application of specific parasitic molecules in regulating autoimmune responses remains to be explored. Here we report on the immune modulatory function of Lacto-N-fucopentaose III (LNFPIII), a schistosome glycan, in an animal model for multiple sclerosis. We found that LNFPIII treatment significantly reduced the severity of experimental autoimmune encephalomyelitis (EAE) and CNS inflammation, and skewed peripheral immune response to a Th2 dominant profile. Inflammatory monocytes (IMCs) purified from LNFPIII-treated mice had incr...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5625216</comments>
            <pubDate>Fri, 30 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5625216</guid>        </item>
        <item>
            <title>Oxidative stress and endosome recycling are complementary mechanisms reorganizing the T-cell receptor signaling complex in SLE.</title>
            <link>http://www.medworm.com/index.php?rid=5605030&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22245265%26dopt%3DAbstract</link>
            <description>Authors: Perl A
    PMID: 22245265 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605030</comments>
            <pubDate>Fri, 30 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5605030</guid>        </item>
        <item>
            <title>DNA-responsive inflammasomes and their regulators in autoimmunity.</title>
            <link>http://www.medworm.com/index.php?rid=5605031&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22245264%26dopt%3DAbstract</link>
            <description>Authors: Choubey D
    Abstract
    Upon sensing microbial and self-derived DNA, DNA sensors initiate innate immune responses. These sensors include the interferon (IFN)-inducible Toll-like receptor 9 (TLR9) and PYHIN proteins. Upon sensing DNA, cytosolic (murine Aim2 and human AIM2) and nuclear (IFI16) PYHIN proteins recruit an adaptor protein (ASC) and pro-caspase-1 to form an inflammasome, which activates caspase-1. The activated caspase-1 cleaves pro-IL-1β and pro-IL-18 to generate active forms. However, upon sensing cytosolic DNA, the IFI16 protein recruits STING to induce the expression of type I IFN. Recognition of self DNA by innate immune cells contributes to the production of increased levels of type I IFN. Given that the type I IFNs modulate the expression of inflammasome prote...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605031</comments>
            <pubDate>Thu, 29 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5605031</guid>        </item>
        <item>
            <title>Combination therapy with InsB9-23 peptide immunization and CTLA4-IgG does not reverse diabetes in NOD mice.</title>
            <link>http://www.medworm.com/index.php?rid=5605034&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22239953%26dopt%3DAbstract</link>
            <description>Authors: Schneider DA, Sarikonda G, von Herrath MG
    PMID: 22239953 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605034</comments>
            <pubDate>Fri, 23 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5605034</guid>        </item>
        <item>
            <title>Phenotype and function of dendritic cells of patients with systemic lupus erythematosus.</title>
            <link>http://www.medworm.com/index.php?rid=5605033&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22239954%26dopt%3DAbstract</link>
            <description>Authors: Crispín JC, Vargas-Rojas MI, Monsiváis-Urenda A, Alcocer-Varela J
    Abstract
    Dendritic cells (DC) regulate the activation and differentiation of T cells. They are activated by signals of inflammation and tissue damage, and thus could play a role in the amplification and perpetuation of autoimmune diseases such as systemic lupus erythematosus (SLE). Here we analyzed the phenotype of circulating DC from patients with SLE and studied their differentiation from monocytes. Peripheral blood DC exhibited increased levels of activation in patients with SLE. Although their in vitro differentiation process occurred normally, their responses to activation stimuli (LPS, TNF-α plus PGE(2), anti-CD40) were abnormal when compared to DC differentiated from healthy monocytes. When incubat...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605033</comments>
            <pubDate>Thu, 22 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5605033</guid>        </item>
        <item>
            <title>Chronic Rotavirus Infection in an Infant with Severe Combined Immunodeficiency: Successful Treatment by Hematopoietic Stem Cell Transplantation.</title>
            <link>http://www.medworm.com/index.php?rid=5605032&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22244360%26dopt%3DAbstract</link>
            <description>Authors: Patel NC, Hertel PM, Hanson IC, Krance RA, Crawford SE, Estes M, Paul ME
    PMID: 22244360 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605032</comments>
            <pubDate>Thu, 22 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5605032</guid>        </item>
        <item>
            <title>Thymic function after allogeneic stem cell transplantation is dependent on graft source and predictive of long term survival.</title>
            <link>http://www.medworm.com/index.php?rid=5579166&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22227522%26dopt%3DAbstract</link>
            <description>Authors: Sairafi D, Mattsson J, Uhlin M, Uzunel M
    Abstract
    T-cell deficiency after allogeneic stem cell transplantation (ASCT) is common and has major impact on clinical outcome. In this retrospective study 210 patients were analyzed with regards to levels of T-cell receptor excision circles (TRECs) during the first 24months after transplantation. We could for the first time show a significant correlation between the use of bone marrow grafts and higher TREC levels &amp;gt;6months post-ASCT (p&amp;lt;0.001). Treatment with anti-thymocyte globulin was correlated with lower TREC levels ≤6months post-ASCT (p&amp;lt;0.001). Patients with TREC levels above median at 3months had a superior overall survival, 80% vs. 56% (p=0.002), and lower transplantation-related mortality, 7% vs. 21% (p=0.01). We...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579166</comments>
            <pubDate>Fri, 16 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5579166</guid>        </item>
        <item>
            <title>Blistering insights into the pathogenesis of bullous pemphigoid.</title>
            <link>http://www.medworm.com/index.php?rid=5579169&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22217422%26dopt%3DAbstract</link>
            <description>Authors: Wong HK, Bechtel MA
    PMID: 22217422 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579169</comments>
            <pubDate>Tue, 13 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5579169</guid>        </item>
        <item>
            <title>IL-10-generated tolerogenic dendritic cells are optimal for functional regulatory T cell induction - A comparative study of human clinical-applicable DC.</title>
            <link>http://www.medworm.com/index.php?rid=5579167&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22225835%26dopt%3DAbstract</link>
            <description>Authors: Boks MA, Kager-Groenland JR, Haasjes MS, Zwaginga JJ, van Ham SM, Ten Brinke A
    Abstract
    Tolerogenic dendritic cells (tDC) are a promising tool for specific cellular therapy to induce immunological tolerance in transplantation and autoimmunity. To date, most described tDC methods have not been converted into clinically applicable protocols and systematic comparison of required functional characteristics, i.e. migration and functional regulatory T cell (Treg) induction, is lacking. We compare clinical-grade tDC generated with vitamin D(3), IL-10, dexamethasone, TGFβ or rapamycin. For good migratory capacity and a stable phenotype, additional maturation of tDC was required. Maturation with a cocktail of TNFα, IL-1β and PGE(2) induced optimal migration. Importantly, all tDC...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579167</comments>
            <pubDate>Sat, 10 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5579167</guid>        </item>
        <item>
            <title>Effect of HLA DR epitope de-immunization of Factor VIII in vitro and in vivo.</title>
            <link>http://www.medworm.com/index.php?rid=5579168&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22222093%26dopt%3DAbstract</link>
            <description>Authors: Moise L, Song C, Martin WD, Tassone R, De Groot AS, Scott DW
    Abstract
    T cell-dependent development of anti-Factor VIII (FVIII) antibodies that neutralize FVIII activity is a major obstacle to replacement therapy in hemophilia A. To create a less immunogenic therapeutic protein, recombinant FVIII can be modified to reduce HLA binding of epitopes based on predicted anchoring residues. Here, we used immunoinformatic tools to identify C2 domain HLA DR epitopes and predict site-specific mutations that reduce immunogenicity. Epitope peptides corresponding to original and modified sequences were validated in HLA binding assays and in immunizations of hemophilic E16 mice, DR3 and DR4 mice and DR3×E16 mice. Consistent with immunoinformatic predictions, original epitopes are immuno...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579168</comments>
            <pubDate>Thu, 08 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5579168</guid>        </item>
        <item>
            <title>Therapeutic strategies in multiple sclerosis.</title>
            <link>http://www.medworm.com/index.php?rid=5536992&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22155340%26dopt%3DAbstract</link>
            <description>Authors: Comabella M, Khoury SJ
    PMID: 22155340 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5536992</comments>
            <pubDate>Fri, 02 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5536992</guid>        </item>
        <item>
            <title>The ion channel network in T lymphocytes, a target for immunotherapy.</title>
            <link>http://www.medworm.com/index.php?rid=5536989&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22189042%26dopt%3DAbstract</link>
            <description>Authors: Conforti L
    PMID: 22189042 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5536989</comments>
            <pubDate>Fri, 02 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5536989</guid>        </item>
        <item>
            <title>Interleukin-33 upregulation in peripheral leukocytes and CNS of multiple sclerosis patients.</title>
            <link>http://www.medworm.com/index.php?rid=5536988&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22189043%26dopt%3DAbstract</link>
            <description>Authors: Christophi GP, Gruber RC, Panos M, Christophi RL, Jubelt B, Massa PT
    Abstract
    Multiple sclerosis (MS) is an immune-mediated demyelinating disease of the central nervous system (CNS). Here we document for the first time that the cytokine IL-33 is upregulated in both the periphery and the CNS of MS patients. Plasma IL-33 was elevated in MS patients compared to normal subjects and a three-month treatment of MS patients with interferon β-1a resulted in a significant decrease of IL-33 levels. Similarly, stimulated cultured lymphocytes and macrophages from MS patients had elevated IL-33 levels compared to normal subjects. In parallel, the transcription factor NF-κB that mediates IL-33 transcription was also elevated in leukocytes of MS patients. IL-33 was elevated in normal-ap...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5536988</comments>
            <pubDate>Fri, 02 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5536988</guid>        </item>
        <item>
            <title>Galectin-9 signaling prolongs survival in murine lung-cancer by inducing macrophages to differentiate into plasmacytoid dendritic cell-like macrophages.</title>
            <link>http://www.medworm.com/index.php?rid=5536991&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22177847%26dopt%3DAbstract</link>
            <description>Authors: Kadowaki T, Arikawa T, Shinonaga R, Oomizu S, Inagawa H, Soma G, Niki T, Hirashima M
    Abstract
    Galectin-9 (Gal-9) expanded plasmacytoid dendritic cell-like macrophages (pDC-Mϕs) in lung cancer-bearing mice and prolonged the survival. Gal-9 increased the frequency of CD11c(high) cells in M-CSF- but not GM-CSF-induced Mϕs in vitro in a Tim-3 independent manner. CD11c(high) cells differentiated with M-CSF+Gal-9 expressed pDC-Mϕ markers, such as PDCA-1 and F4/80. These cells expressed high TLR7, TLR8 and TLR9, although they exhibited decreased IFN-α mRNA levels. LPS or LLC stimulation further elevated pDC-Mϕ markers, indicating that M-CSF+Gal-9-induced Mϕs were pDC-Mϕ precursors. Moreover, LPS stimulation resulted in the increased IRF7 and E2-2 levels, suggesting that th...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5536991</comments>
            <pubDate>Fri, 25 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5536991</guid>        </item>
        <item>
            <title>Lipopolysaccharide mediated mast cells induce IL-10 producing regulatory T Cells through the ICOSL/ICOS axis.</title>
            <link>http://www.medworm.com/index.php?rid=5536993&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22154192%26dopt%3DAbstract</link>
            <description>This study provided new evidence for the regulatory role of MCs.
    PMID: 22154192 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5536993</comments>
            <pubDate>Sun, 20 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5536993</guid>        </item>
        <item>
            <title>A phase I/IIa immunotherapy trial of HIV-1-infected patients with Tat, Rev and Nef expressing dendritic cells followed by treatment interruption.</title>
            <link>http://www.medworm.com/index.php?rid=5536990&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22177848%26dopt%3DAbstract</link>
            <description>Authors: Allard SD, De Keersmaecker B, de Goede AL, Verschuren EJ, Koetsveld J, Reedijk ML, Wylock C, De Bel AV, Vandeloo J, Pistoor F, Heirman C, Beyer WE, Eilers PH, Corthals J, Padmos I, Thielemans K, Osterhaus AD, Lacor P, der Ende ME, Aerts JL, van Baalen CA, Gruters RA
    Abstract
    In a phase I/IIa clinical trial, 17 HIV-1 infected patients, stable on cART, received 4 vaccinations with autologous dendritic cells electroporated with mRNA encoding Tat, Rev and Nef, after which cART was interrupted. Vaccination was safe and feasible. During the analytical treatment interruption (ATI), no serious adverse events were observed. Ninety-six weeks following ATI, 6/17 patients remained off therapy. Although induced and/or enhanced CD4(+) and CD8(+) T-cell responses specific for the immunog...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5536990</comments>
            <pubDate>Wed, 16 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5536990</guid>        </item>
        <item>
            <title>Tolerance induced by anti-DNA Ig peptide in (NZB×NZW)F(1) lupus mice impinges on the resistance of effector T cells to suppression by regulatory T cells.</title>
            <link>http://www.medworm.com/index.php?rid=5494380&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22137928%26dopt%3DAbstract</link>
            <description>Authors: Yu Y, Liu Y, Shi FD, Zou H, Hahn BH, La Cava A
    Abstract
    We have previously shown that immune tolerance induced by the anti-DNA Ig peptide pCons in (NZB×NZW)F(1) (NZB/W) lupus mice prolonged survival of treated animals and delayed the appearance of autoantibodies and glomerulonephritis. Part of the protection conferred by pCons could be ascribed to the induction of regulatory T cells (T(Reg)) that suppressed the production of anti-DNA antibodies in a p38 MAPK-dependent fashion. Here we show that another effect of pCons in the induction of immune tolerance in NZB/W lupus mice is the facilitation of effector T cell suppression by T(Reg). These new findings indicate that pCons exerts protective effects in NZB/W lupus mice by differentially modulating the activity of different...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5494380</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5494380</guid>        </item>
        <item>
            <title>The relevance of photopheresis to autoreactive diseases.</title>
            <link>http://www.medworm.com/index.php?rid=5494381&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22134055%26dopt%3DAbstract</link>
            <description>Authors: Samimi S, Rook AH
    PMID: 22134055 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5494381</comments>
            <pubDate>Fri, 11 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5494381</guid>        </item>
        <item>
            <title>Activated iNKT cells promote Vγ9Vδ2-T cell anti-tumor effector functions through the production of TNF-α</title>
            <link>http://www.medworm.com/index.php?rid=5458638&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22122798%26dopt%3DAbstract</link>
            <description>Authors: Schneiders FL, de Bruin RC, Santegoets SJ, Bonneville M, Scotet E, Scheper RJ, Verheul HM, de Gruijl TD, van der Vliet HJ
    Abstract
    Vγ9Vδ2-T cells constitute a proinflammatory lymphocyte subpopulation with established antitumor activity. Phosphoantigens activate Vγ9Vδ2-T cells in vivo and in vitro. We studied whether the antitumor activity of Vγ9Vδ2-T cells can be potentiated by invariant NKT cells (iNKT), an important immunoregulatory T cell subset. When activated by the glycolipid α-galactosylceramide (α-GalCer), iNKT produce large amounts of cytokines involved in antitumor immune responses. Monocyte-derived dendritic cells were loaded with both phosphoantigens (using aminobisphosphonates) and α-GalCer during maturation and subsequently co-cultured with Vγ9Vδ2-...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5458638</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5458638</guid>        </item>
        <item>
            <title>Increased risk of asthma and atopic dermatitis in perinatally HIV-infected children and adolescents.</title>
            <link>http://www.medworm.com/index.php?rid=5424204&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22094294%26dopt%3DAbstract</link>
            <description>Authors: Siberry GK, Leister E, Jacobson DL, Foster SB, Seage GR, Lipshultz SE, Paul ME, Purswani M, Colin AA, Scott G, Shearer WT
    Abstract
    The incidence of asthma and atopic dermatitis (AD) was evaluated in HIV-infected (n=451) compared to HIV-exposed (n=227) but uninfected (HEU) children and adolescents by abstraction from clinical charts. Asthma was more common in HIV-infected compared to HEU children by clinical diagnosis (25% vs. 20%, p=0.101), by asthma medication use, (31% vs. 22%, p=0.012), and by clinical diagnosis and/or medication use, (34% vs. 25%, p=0.012). HIV-infected children had a greater risk of asthma compared to HEU children (HR=1.37, 95% CI: 1.01 to 1.86). AD was more common in HIV-infected than HEU children (20% vs. 12%, p=0.009)) and children with AD were mor...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5424204</comments>
            <pubDate>Sun, 30 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5424204</guid>        </item>
        <item>
            <title>Targeted immunosuppression: No longer naïve.</title>
            <link>http://www.medworm.com/index.php?rid=5424205&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22079331%26dopt%3DAbstract</link>
            <description>Authors: Hagan RS, Powell JD
    PMID: 22079331 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5424205</comments>
            <pubDate>Tue, 25 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5424205</guid>        </item>
        <item>
            <title>Development of IgA nephropathy-like glomerulonephritis associated with Wiskott-Aldrich syndrome protein deficiency.</title>
            <link>http://www.medworm.com/index.php?rid=5424206&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22079330%26dopt%3DAbstract</link>
            <description>We examined whether increased aberrant IgA production is associated with the development of glomerulonephritis in WASp-deficient mice. Serum IgA and IgA production by splenic B cells was increased in WASp-deficient mice compared to wild-type (WT) mice. A lectin-binding study revealed a reduced ratio of sialylated and galactosylated IgA in the sera from old WASp-deficient mice. Circulating IgA-containing immune complexes showed significantly higher titers in WASp-deficient mice compared to WT mice. These results indicate that the increased IgA production and aberrant glycosylation of IgA may be critically involved in the pathogenesis of glomerulonephritis in WAS.
    PMID: 22079330 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5424206</comments>
            <pubDate>Wed, 19 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5424206</guid>        </item>
        <item>
            <title>Noncollagenous 16A domain of type XVII collagen-reactive CD4(+) T cells play a pivotal role in the development of active disease in experimental bullous pemphigoid model.</title>
            <link>http://www.medworm.com/index.php?rid=5382215&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22044750%26dopt%3DAbstract</link>
            <description>Authors: Ujiie H, Shibaki A, Nishie W, Shinkuma S, Moriuchi R, Qiao H, Shimizu H
    Abstract
    Bullous pemphigoid (BP), the most common autoimmune blistering disease, is caused by autoantibodies against type XVII collagen (COL17). We recently demonstrated that CD4(+) T cells were crucial for the production of anti-COL17 IgG and for the development of the BP phenotype by using a novel active BP mouse model by adoptively transferring immunized splenocytes into immunodeficient COL17-humanized mice. Noncollagenous 16A (NC16A) domain of COL17 is considered to contain the main pathogenic epitopes of BP, however, the pathogenicity of COL17 NC16A-reactive CD4(+) T cells has never been elucidated. To address this issue, we modulated the immune responses against COL17 in active BP model by using ...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382215</comments>
            <pubDate>Mon, 17 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382215</guid>        </item>
        <item>
            <title>The anti-microbial peptide LL-37 modulates immune responses in the palatine tonsils where it is exclusively expressed by neutrophils and a subset of dendritic cells.</title>
            <link>http://www.medworm.com/index.php?rid=5382217&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22036268%26dopt%3DAbstract</link>
            <description>Authors: Sigurdardottir SL, Thorleifsdottir RH, Guzman AM, Gudmundsson GH, Valdimarsson H, Johnston A
    Abstract
    Antimicrobial peptides are essential elements of epithelial defense against invading micro-organisms. The palatine tonsils are positioned at the entry of the airway and the gut and as such are ideally situated to act as immune sentinels in the pharynx protecting against microbial invasion. Tonsils express a number of antimicrobial peptides including hCAP18/LL-37. Here we clearly define the expression of hCAP18/LL-37 in the tonsils showing unequivocally that hCAP18/LL-37 is mainly expressed by infiltrating neutrophils and follicular CD11c+CD13+HLA-DR+ dendritic cells, rarely by macrophages, and never by the epithelium itself. To explore possible functions for follicle-deriv...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382217</comments>
            <pubDate>Fri, 07 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382217</guid>        </item>
        <item>
            <title>Immunomodulatory effects of extracorporeal photochemotherapy in systemic sclerosis.</title>
            <link>http://www.medworm.com/index.php?rid=5382216&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22036269%26dopt%3DAbstract</link>
            <description>Authors: Papp G, Horvath IF, Barath S, Gyimesi E, Vegh J, Szodoray P, Zeher M
    Abstract
    The aim of this study was to evaluate the clinical and immunomodulatory effects of extracorporeal photochemotherapy (ECP) in systemic sclerosis (SSc). We enrolled 16 patients with diffuse cutaneous SSc, who received 12 ECP treatments in total. After ECP treatments, the dermal thickness reduced and the mobility of joints improved. Internal organ involvement did not deteriorate. The percentages and numbers of peripheral Th17 cells decreased, the values of Tr1 and Treg cells increased, and the suppressor capacity of Treg cells improved. Interestingly, we found a positive correlation between the reduction of IL-17 levels and skin thickness measured by ultrasound. Moreover, levels of CCL2 and TGF-beta...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382216</comments>
            <pubDate>Fri, 07 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382216</guid>        </item>
        <item>
            <title>Galectin-1 research in T cell immunity: Past, present and future.</title>
            <link>http://www.medworm.com/index.php?rid=5382218&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22019770%26dopt%3DAbstract</link>
            <description>Authors: Cedeno-Laurent F, Dimitroff CJ
    Abstract
    Galectin-1 (Gal-1) is one of 15 evolutionarily conserved ß-galactoside-binding proteins that display biologically-diverse activities in pathogenesis of inflammation and cancer. Gal-1 is variably expressed on immune cells and endothelial cells, though is commonly found and secreted at high levels in cancer cells. It induces apoptosis in effector T cells through homodimeric binding of N-acetyllactosamines on membrane glycoproteins (Gal-1 ligands). There is also compelling evidence in models of cancer and autoimmunity that recombinant Gal-1 (rGal-1) can potentiate immunoregulatory function of T cells. Here, we review Gal-1's structural and functional features, while analyzing potential drawbacks and technical difficulties inherent to r...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382218</comments>
            <pubDate>Thu, 06 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382218</guid>        </item>
        <item>
            <title>MAP3738c and MptD are specific tags of Mycobacterium avium subsp. paratuberculosis infection in type I diabetes mellitus.</title>
            <link>http://www.medworm.com/index.php?rid=5282679&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21664191%26dopt%3DAbstract</link>
            <description>Authors: Cossu A, Rosu V, Paccagnini D, Cossu D, Pacifico A, Sechi LA
    Abstract
    Mycobacterium avium subsp. paratuberculosis (Map) is the causative agent of Johne's disease, a chronic inflammation of ruminants' intestine. Recent studies have linked Map to type I Diabetes mellitus (T1DM). We searched the presence of antibodies against two specific proteins of Map (MptD and MAP3738c) in sera of patients affected by T1DM and type II Diabetes mellitus (T2DM). MptD protein (MAP3733c) has been recognized as a Map virulent factor whereas MAP3738c has not yet been studied. Both proteins are encoded by genes belonging to a Map specific pathogenicity island. Forty three T1DM patients' sera, 56 T2DM patients' sera and 48 healthy subjects' sera were screened by ELISA to evaluate the immunorespon...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5282679</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5282679</guid>        </item>
        <item>
            <title>Assessing immune function by profiling cytokine release from stimulated blood leukocytes and the risk of infection in rheumatoid arthritis.</title>
            <link>http://www.medworm.com/index.php?rid=5282678&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21703930%26dopt%3DAbstract</link>
            <description>Authors: Krause ML, Davis JM, Knutson KL, Strausbach MA, Crowson CS, Therneau TM, Wettstein PJ, Matteson EL, Gabriel SE
    Abstract
    Persons with rheumatoid arthritis (RA) suffer a high burden of infections, but currently no biomarkers are available to identify individuals at greatest risk. A prospective longitudinal study was therefore conducted to determine the association between the responsiveness of ex vivo cytokine production and 6-month risk of infections. Infections were identified by billing codes and validated by medical record review. At baseline, the release of 17 cytokines by peripheral blood mononuclear cells in response to stimulation, or media alone, was measured using multiplexed cytokine analysis. Production of IL-2, IL-8, IL-10, IL-17, TNF-α, IFN-γ, and GM-CSF, ind...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5282678</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5282678</guid>        </item>
        <item>
            <title>Efficacy and safety of Hizentra(®) in patients with primary immunodeficiency after a dose-equivalent switch from intravenous or subcutaneous replacement therapy.</title>
            <link>http://www.medworm.com/index.php?rid=5282677&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21705277%26dopt%3DAbstract</link>
            <description>Authors: Jolles S, Bernatowska E, de Gracia J, Borte M, Cristea V, Peter HH, Belohradsky BH, Wahn V, Neufang-Hüber J, Zenker O, Grimbacher B
    Abstract
    A prospective, open-label, multicenter, single-arm, Phase III study evaluated the efficacy and safety of Hizentra(®), a 20% human IgG for subcutaneous administration, in 51 primary immunodeficiency patients over 40weeks. Patients previously on intravenous or subcutaneous IgG were switched to weekly subcutaneous infusions of Hizentra(®) at doses equivalent to their previous treatment. IgG levels achieved with Hizentra(®) were similar to pre-study levels with subcutaneous, and higher by 17.7% than pre-study levels with intravenous IgG. No serious bacterial infections were reported in the efficacy period. The rate of all infections w...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5282677</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5282677</guid>        </item>
        <item>
            <title>Epitope mapping of antibodies to VlsE protein of Borrelia burgdorferi in post-Lyme disease syndrome.</title>
            <link>http://www.medworm.com/index.php?rid=5282676&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21778118%26dopt%3DAbstract</link>
            <description>Authors: Chandra A, Latov N, Wormser GP, Marques AR, Alaedini A
    Abstract
    The VlsE lipoprotein of Borrelia burgdorferi elicits a strong immune response during the course of Lyme disease. The present study was aimed at characterization of the epitopes of VlsE targeted by the antibody response in patients with post-Lyme disease syndrome, a condition characterized by persisting symptoms of pain, fatigue, and/or neurocognitive impairment despite antibiotic treatment of B. burgdorferi infection. Epitope mapping was carried out using microarrays that contained synthesized overlapping peptides covering the full sequence of VlsE from B. burgdorferi B31. In addition to the previously characterized IR6 region in the variable domain, specific sequences in the N- and C-terminal invariable domai...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5282676</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5282676</guid>        </item>
        <item>
            <title>Identification of FOXP3-negative regulatory T-like (CD4(+)CD25(+)CD127(low)) cells in patients with immune dysregulation, polyendocrinopathy, enteropathy, X-linked syndrome.</title>
            <link>http://www.medworm.com/index.php?rid=5282675&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21802372%26dopt%3DAbstract</link>
            <description>Authors: Otsubo K, Kanegane H, Kamachi Y, Kobayashi I, Tsuge I, Imaizumi M, Sasahara Y, Hayakawa A, Nozu K, Iijima K, Ito S, Horikawa R, Nagai Y, Takatsu K, Mori H, Ochs HD, Miyawaki T
    Abstract
    Immune dysregulation, polyendocrinopathy, enteropathy, X-linked (IPEX) syndrome is an autoimmune disorder caused by mutations in the FOXP3 gene, which plays a key role in the generation of CD4(+)CD25(+)regulatory T (Treg) cells. We selected CD127 as the surface marker of Treg cells to illustrate the development and function of Treg cells in IPEX syndrome. CD4(+)CD25(+)FOXP3(+) T cells, the putative Treg cells, were almost completely absent in all patients. Importantly, a substantial number of CD4(+)CD25(+)CD127(low) T cells were observed in 3 IPEX patients with hypomorphic mutations in the F...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5282675</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5282675</guid>        </item>
        <item>
            <title>RAGE against the self.</title>
            <link>http://www.medworm.com/index.php?rid=5282674&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21889912%26dopt%3DAbstract</link>
            <description>Authors: Darrasse-Jèze G
    PMID: 21889912 [PubMed - in process] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5282674</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5282674</guid>        </item>
        <item>
            <title>Regulatory T-like cells: Another variation on the theme of hypomorphic mutations?</title>
            <link>http://www.medworm.com/index.php?rid=5282671&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21955568%26dopt%3DAbstract</link>
            <description>Authors: Notarangelo LD
    PMID: 21955568 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5282671</comments>
            <pubDate>Fri, 16 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5282671</guid>        </item>
        <item>
            <title>Integrating clinical perspectives into graduate education.</title>
            <link>http://www.medworm.com/index.php?rid=5282673&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21944668%26dopt%3DAbstract</link>
            <description>Authors: Henrickson SE, Agyemang AF, Garg S, Hafler JP
    PMID: 21944668 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5282673</comments>
            <pubDate>Mon, 05 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5282673</guid>        </item>
        <item>
            <title>Administering human adipose-derived mesenchymal stem cells to prevent and treat experimental arthritis.</title>
            <link>http://www.medworm.com/index.php?rid=5282672&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21944669%26dopt%3DAbstract</link>
            <description>In this study, we examined whether hASCs could play a protective and/or therapeutic role in collagen-induced arthritis (CIA). We showed that hASCs both prevented and treated CIA by significantly reducing the incidence and severity of experimental arthritis. We further demonstrated that treatment with hASCs inhibited the production of various inflammatory mediators, decreased antigen-specific Th1/Th17 cell expansion, and induced the production of anti-inflammatory cytokine interleukin-10. Moreover, hASCs could induce the generation of antigen-specific Treg cells with the capacity to suppress collagen-specific T cell responses.
    PMID: 21944669 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5282672</comments>
            <pubDate>Fri, 02 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5282672</guid>        </item>
        <item>
            <title>The comprehensive assessment of local immune status of ovarian cancer by the clustering of multiple immune factors.</title>
            <link>http://www.medworm.com/index.php?rid=5282670&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21955569%26dopt%3DAbstract</link>
            <description>In conclusion the comprehensive analysis of local immune status led to subdivide ovarian cancers into groups with better or worse prognoses and may guide precise understanding of the local immunity.
    PMID: 21955569 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5282670</comments>
            <pubDate>Fri, 02 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5282670</guid>        </item>
        <item>
            <title>Characterization of Zaire ebolavirus glycoprotein-specific monoclonal antibodies.</title>
            <link>http://www.medworm.com/index.php?rid=5249395&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21925951%26dopt%3DAbstract</link>
            <description>In this study, recombinant VSVΔG/ZEBOVGP was used to generate monoclonal antibodies (MAbs) against the ZEBOV GP. A total of 8 MAbs were produced using traditional hybridoma cell fusion technology, and then characterized by ELISA using ZEBOV VLPs, Western blotting, an immunofluorescence assay, and immunoprecipitation. All 8 MAbs worked in IFA and IP, suggesting that they are all conformational MAbs, however six of them recognized linearized epitopes by WB. ELISA results demonstrated that one MAb bound to a secreted GP (sGP 1-295aa); three bind to a part of the mucin domain (333-458aa); three MAbs recognized epitopes on the C-terminal domain of GP1 (296-501aa); and one bound to full length GP (VLPs/GP1,2 ΔTm). Using a mouse model these MAbs were evaluated for their therapeutic capacity dur...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5249395</comments>
            <pubDate>Wed, 31 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5249395</guid>        </item>
        <item>
            <title>Chronic non-bacterial osteomyelitis is associated with impaired Sp1 signaling, reduced IL10 promoter phosphorylation, and reduced myeloid IL-10 expression.</title>
            <link>http://www.medworm.com/index.php?rid=5249394&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21925952%26dopt%3DAbstract</link>
            <description>Authors: Hofmann SR, Schwarz T, Möller JC, Morbach H, Schnabel A, Rösen-Wolff A, Girschick HJ, Hedrich CM
    Abstract
    Chronic non-bacterial osteomyelitis (CNO) is an auto-inflammatory disorder that affects the skeletal system. Interleukin (IL-)10 is an immune-modulatory cytokine that controls inflammation, and limits inflammatory cytokine responses. Dysregulation of IL-10 expression has been shown to result in autoimmune and infectious diseases. We investigated IL-10 expression by monocytic cells from CNO patients and controls. In response to stimulation with LPS, IL-10 expression from CNO monocytes was reduced (p&amp;lt;0.001). This was independent of IL10 promoter polymorphisms. Thus, we investigated Sp1 recruitment to the IL10 promoter and saw markedly reduced binding in CNO monocyte...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5249394</comments>
            <pubDate>Tue, 30 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5249394</guid>        </item>
        <item>
            <title>Anti-FcεR1 antibody injections activate basophils and mast cells and delay Type 1 diabetes onset in NOD mice.</title>
            <link>http://www.medworm.com/index.php?rid=5234360&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21920822%26dopt%3DAbstract</link>
            <description>Authors: Hübner MP, Larson D, Torrero MN, Mueller E, Shi Y, Killoran KE, Mitre E
    Abstract
    Mounting evidence suggests that helminth infections protect against autoimmune diseases. As helminths cause chronic IgE-mediated activation of basophils and mast cells we hypothesized that continuous activation of these cells could prevent diabetes onset in nonobese diabetic (NOD) mice in the absence of infection. Anti-FcεR1 activated basophils and mast cells and resulted in the release of IL-4 and histamine into the bloodstream. Anti-FcεR1-treated NOD mice showed a type 2 shift in insulin-specific antibody production and exhibited significant delays in diabetes onset. IL-4 responses played a partial role as the protective effect of anti-FcεR1 therapy was diminished in IL-4-deficient NOD m...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5234360</comments>
            <pubDate>Tue, 23 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5234360</guid>        </item>
        <item>
            <title>A network of regulatory pathways in lepromatous leprosy.</title>
            <link>http://www.medworm.com/index.php?rid=5220266&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21903479%26dopt%3DAbstract</link>
            <description>Authors: Abbas AK
    PMID: 21903479 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5220266</comments>
            <pubDate>Thu, 18 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5220266</guid>        </item>
        <item>
            <title>DOCK8 deficiency, T cell receptor excision circles and newborn screening.</title>
            <link>http://www.medworm.com/index.php?rid=5220267&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21875821%26dopt%3DAbstract</link>
            <description>Authors: Fuleihan RL
    PMID: 21875821 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5220267</comments>
            <pubDate>Sun, 07 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5220267</guid>        </item>
        <item>
            <title>The decidual gamma-delta T cells up-regulate the biological functions of trophoblasts via IL-10 secretion in early human pregnancy.</title>
            <link>http://www.medworm.com/index.php?rid=5179470&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21873118%26dopt%3DAbstract</link>
            <description>Authors: Fan DX, Duan J, Li MQ, Xu B, Li DJ, Jin LP
    Abstract
    The functions of decidual γδT cells in early human pregnancy are not fully understood. The present study was undertaken to characterize the action of decidual γδT cells, and analyze their regulatory roles in proliferation and invasion of trophoblasts in early human pregnancy. It was revealed that decidual γδT cells were a CD4(-) and CD8(-) subset whose numbers increased significantly in either the decidua or peripheral blood. The main cytokines synthesized in decidual γδT cells in decreasing concentration were; IL-10&amp;gt;TGF-β&amp;gt;TNF-α≥IFN-γ, with little IL-2 or IL-4 being produced. Decidual γδT cells promoted trophoblast proliferation and invasion, and suppressed trophoblast apoptosis through IL-10 secretio...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5179470</comments>
            <pubDate>Sat, 06 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5179470</guid>        </item>
        <item>
            <title>Analysis of bulk and virus-specific CD8+ T cells reveals advanced differentiation of CD8+ T cells in patients with common variable immunodeficiency.</title>
            <link>http://www.medworm.com/index.php?rid=5179471&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21873117%26dopt%3DAbstract</link>
            <description>Authors: Kuntz M, Goldacker S, Blum HE, Pircher H, Stampf S, Peter HH, Thimme R, Warnatz K
    Abstract
    Common variable immunodeficiency (CVID) is a heterogeneous antibody deficiency syndrome with alterations in T cell regulation and function in a subgroup of patients. We assessed phenotype and function of bulk and virus-specific CD8+ T cells of a cohort of 34 HLA-A2+ CVID patients by pentamer technology and flow cytometry in relationship to their immunological and clinical phenotypes. Bulk CD8+ T cells displayed a shift toward a more antigen experienced and activated differentiation state. The advanced differentiation pattern was mainly found in a subgroup of CVID patients with lymphadenopathy and granulomatous disease. This effect existed independently of the patients' CMV status eve...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5179471</comments>
            <pubDate>Thu, 04 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5179471</guid>        </item>
        <item>
            <title>HIV controllers: A multifactorial phenotype of spontaneous viral suppression.</title>
            <link>http://www.medworm.com/index.php?rid=5158333&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21865089%26dopt%3DAbstract</link>
            <description>Authors: Thèze J, Chakrabarti LA, Vingert B, Porichis F, Kaufmann DE
    Abstract
    A small minority of HIV-infected individuals, known as HIV controllers, is able to exert long-term control over HIV replication in the absence of treatment. Increasing evidence suggests that the adaptive immune system plays a critical role in this control but also that a combination of several host and/or viral factors, rather than a single cause, leads to this rare phenotype. Here, we review recent advances in the study of these remarkable individuals. We summarize the epidemiology and clinical characteristics of HIV controllers, and subsequently describe contributing roles of host genetic factors, innate and adaptive immune responses, and viral factors to this phenotype. We emphasize distinctive charac...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5158333</comments>
            <pubDate>Wed, 03 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5158333</guid>        </item>
        <item>
            <title>Therapeutic in vivo selection of thymic-derived natural T regulatory cells following non-myeloablative hematopoietic stem cell transplant for IPEX.</title>
            <link>http://www.medworm.com/index.php?rid=5158332&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21865090%26dopt%3DAbstract</link>
            <description>We describe a child diagnosed with IPEX who underwent a reduced intensity, T and B cell depleted, matched unrelated donor bone marrow transplant followed by clinical resolution. Using lineage-specific donor chimerism studies, we demonstrate that non-myeloablative HSCT resolves disease in the context of low level donor hematopoietic stem cell (HSC) engraftment. Despite low-levels of donor HSC, thymically-derived nTreg and to a lesser extent CD4(+) and CD8(+) T cells, exhibit a selective in vivo growth advantage for populations containing a functional FOXP3 gene. Moreover, nTreg from this patient show regulatory function directly ex vivo. These results have implications for improving clinical therapy for patients with IPEX and provide mechanistic insight into the in vivo development of human...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5158332</comments>
            <pubDate>Mon, 01 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5158332</guid>        </item>
        <item>
            <title>A novel mutation in the coagulation factor 12 gene in subjects with hereditary angioedema and normal C1-inhibitor.</title>
            <link>http://www.medworm.com/index.php?rid=5142210&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21849258%26dopt%3DAbstract</link>
            <description>In this study a novel factor 12 gene mutation, the deletion of 72 base pairs (bp) (c.971_1018+24del72*), was identified in a family of Turkish origin, in two sisters with recurrent skin swellings and abdominal pain attacks and in their symptom-free father. This deletion caused a loss of 48bp of exon 9 (coding amino acids 324* to 340*) in addition to 24bp of intron 9, including the authentic donor splice site of exon 9. The large deletion of 72bp was located in the same F12 gene region as the missense mutations p.Thr328Lys* and p.Thr328Arg* reported previously. Our findings confirm the association between F12 gene mutations modifying the proline-rich region of the FXII protein and hereditary angioedema with normal C1-inhibitor.
    PMID: 21849258 [PubMed - as supplied by publisher] (Source:...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5142210</comments>
            <pubDate>Fri, 29 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5142210</guid>        </item>
        <item>
            <title>Immunopathogenesis of ischemia/reperfusion-associated tissue damage.</title>
            <link>http://www.medworm.com/index.php?rid=5142211&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21839685%26dopt%3DAbstract</link>
            <description>Authors: Ioannou A, Lucca JD, Tsokos GC
    Abstract
    Ischemia/reperfusion (IR) instigates a complex array of inflammatory events which result in damage to the local tissue. IR-related organ damage occurs invariably in several clinical conditions including trauma, organ transplantation, autoimmune diseases and revascularization procedures. We critically review available pre-clinical experimental information on the role of immune response in the expression of tissue damage following IR. Distinct elements of the innate and adaptive immune response are involved in the expression of tissue injury. Interventions such as prevention of binding of natural antibody to antigen expressed on the surface of ischemia-conditioned cells, inhibition of the ensuing complement activation, modulation of To...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5142211</comments>
            <pubDate>Tue, 19 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5142211</guid>        </item>
        <item>
            <title>Prevention of T cell activation by interference of internalized intravenous immunoglobulin (IVIg) with MHC II-dependent native antigen presentation.</title>
            <link>http://www.medworm.com/index.php?rid=5142212&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21824820%26dopt%3DAbstract</link>
            <description>Authors: Aubin E, Proulx DP, Trépanier P, Lemieux R, Bazin R
    Abstract
    Activation of self-reactive CD4(+) T cells plays a central role in the initiation and maintenance of autoimmune diseases. We recently reported that intravenous immunoglobulin (IVIg) inhibits the MHC II-restricted CD4(+) T cell activation induced by the presentation of immune complexes. Because native antigens can also play a role in the induction of several autoimmune diseases, we determined whether IVIg could also affect CD4(+) T cell activation following presentation of native antigens by APCs. Here we report that IVIg significantly reduces the activation of CD4(+) T cells by native ovalbumin. The inhibitory effect is FcγR-independent and occurs following internalization of IVIg inside APCs, where it interfer...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5142212</comments>
            <pubDate>Thu, 07 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5142212</guid>        </item>
        <item>
            <title>Treatment with TNFα blockers induces phenotypical and functional aberrations in peripheral B cells.</title>
            <link>http://www.medworm.com/index.php?rid=5142219&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21334982%26dopt%3DAbstract</link>
            <description>Authors: Karampetsou MP, Andonopoulos AP, Liossis SN
    Abstract
    To dissect the mechanisms of anti-TNFα-induced autoimmunity we examined the phenotype and function of B cells from anti-TNFα-treated patients. Levels of Lyn, Syk, SHP-1, tyrosine 348 phospho-Syk (Y348-Syk) and tyrosine phosphorylated (P-Y) proteins were evaluated and B-cell-surface CD20, CD21 and CD5 were also assessed in 29 patients treated with TNF-α blockers. Following treatment, Lyn, but not Syk or SHP-1, significantly increased particularly in patients with spondyloarthropathies. Increased Lyn levels following treatment correlated with increased Lyn activity as evidenced by a 2.9-fold increase of Y348-Syk (a Lyn target). Peripheral B-cells from 56.3% of the patients displayed a tendency towards increased P-Y leve...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5142219</comments>
            <pubDate>Thu, 30 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5142219</guid>        </item>
        <item>
            <title>Premature ageing of the immune system underlies immunodeficiency in ataxia telangiectasia.</title>
            <link>http://www.medworm.com/index.php?rid=5142218&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21459046%26dopt%3DAbstract</link>
            <description>Authors: Exley AR, Buckenham S, Hodges E, Hallam R, Byrd P, Last J, Trinder C, Harris S, Screaton N, Williams AP, Taylor AM, Shneerson JM
    Abstract
    ATM kinase modulates pathways implicated in premature ageing and ATM genotype predicts survival, yet immunodeficiency in ataxia telangiectasia is regarded as mild and unrelated to age. We address this paradox in a molecularly characterised sequential adult cohort with classical and mild variant ataxia telangiectasia. Immunodeficiency has the characteristics of premature ageing across multiple cellular and molecular immune parameters. This immune ageing occurs without previous CMV infection. Age predicts immunodeficiency in genetically homogeneous ataxia telangiectasia, and in comparison with controls, calendar age is exceeded by immunolo...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5142218</comments>
            <pubDate>Thu, 30 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5142218</guid>        </item>
        <item>
            <title>Tumor necrosis factor alpha (TNF-α) autoregulates its expression and induces adhesion molecule expression in asthma.</title>
            <link>http://www.medworm.com/index.php?rid=5142217&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21459047%26dopt%3DAbstract</link>
            <description>Authors: Babu SK, Puddicombe SM, Arshad HH, Wilson SJ, Ward J, Gozzard N, Higgs G, Holgate ST, Davies DE
    Abstract
    Subjects with mild asthma underwent repeated low-dose allergen exposure and bronchial biopsies were examined for the expression of TNF-α and adhesion molecules. Bronchial biopsies from moderately severe asthmatics were then tested in an explant culture system to assess the effect of Der p and CDP-870, a TNF-α blocking pegylated-antibody Fab, on expression of TNF-α and adhesion molecules. Low-dose allergen challenge significantly upregulated sub-mucosal mast cells, TNF-α(+) cells, and VCAM. When bronchial explants were exposed to Der p and CDP 870 for 24h, CDP 870 caused a significant reduction in TNF-α release both at baseline and following stimulation with Der p a...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5142217</comments>
            <pubDate>Thu, 30 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5142217</guid>        </item>
        <item>
            <title>Role of 2-methoxyestradiol as inhibitor of arthritis and osteoporosis in a model of postmenopausal rheumatoid arthritis.</title>
            <link>http://www.medworm.com/index.php?rid=5142216&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21459677%26dopt%3DAbstract</link>
            <description>Authors: Stubelius A, Andréasson E, Karlsson A, Ohlsson C, Tivesten A, Islander U, Carlsten H
    Abstract
    In postmenopausal rheumatoid arthritis, both the inflammatory disease and estrogen deficiency contribute to the development of osteoporosis. As hormone replacement therapy is no longer an option, we hypothesized that 2-methoxyestradiol (2me2) could be beneficial, and asked if such therapy was associated with effects on reproductive organs. Mice were ovariectomized and arthritis was induced, whereafter mice were administered 2me2, estradiol, or placebo. Clinical and histological scores of arthritis, together with bone mineral density were evaluated. Uteri weight, reactive oxygen species (ROS) from spleen cells, and characterization of cells from joints and lymph nodes were analyze...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5142216</comments>
            <pubDate>Thu, 30 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5142216</guid>        </item>
        <item>
            <title>MASP2 haplotypes are associated with high risk of cardiomyopathy in chronic Chagas disease.</title>
            <link>http://www.medworm.com/index.php?rid=5142215&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21489885%26dopt%3DAbstract</link>
            <description>Authors: Boldt AB, Luz PR, Messias-Reason IJ
    Abstract
    Mannose-binding lectin (MBL) initiates complement on Trypanosoma cruzi through the MBL-associated serine protease 2 (MASP2). We haplotyped six MASP2 polymorphisms in 208 chronic chagasic patients, being 81 indeterminate and 123 symptomatic (76 with cardiac, 19 with digestive and 28 with cardiodigestive forms) and 300 healthy individuals from Southern Brazil, using PCR with sequence-specific primers. The g.1961795C, p.371D diplotype (short CD) occurred at a higher frequency among symptomatic patients, compared with the indeterminate group (P(Bf)=0.012, OR=3.11), as well as genotypes with CD, but not with the g.1945560A in the promoter in cardiac patients (P(Bf)=0.012, OR=13.54). CD haplotypes linked to the p.P126L and p.V377A var...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5142215</comments>
            <pubDate>Thu, 30 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5142215</guid>        </item>
        <item>
            <title>Anti-CD3 mAb treatment cures PDL1-/-.NOD mice of diabetes but precipitates fatal myocarditis.</title>
            <link>http://www.medworm.com/index.php?rid=5142214&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21498129%26dopt%3DAbstract</link>
            <description>Authors: Mfarrej B, Keir M, Dada S, Trikudanathan S, Sayegh MH, Sharpe AH, Guleria I
    Abstract
    Anti-CD3 mAb is an effective therapy that can reverse diabetes in NOD mice and has therapeutic potential in patients with type 1 diabetes (T1D). We administered anti-CD3 to PDL1-/-.NOD mice in order to determine whether this treatment would reverse the development of diabetes in these mice. Mice injected with anti-CD3 mAb neonatally were protected from T1D. However, all of these anti-CD3 mAb treated PDL1-/-.NOD mice developed a wasting disease between 12 and 20 weeks of age with sudden deterioration and weight loss, leading to death within 3-5 days of development of illness. Histology revealed severe inflammation in the heart and skeletal muscles. These results suggest that deficiency of P...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5142214</comments>
            <pubDate>Thu, 30 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5142214</guid>        </item>
        <item>
            <title>Generation of hematopoietic humanized mice in the newborn BALB/c-Rag2null Il2rγnull mouse model: a multivariable optimization approach.</title>
            <link>http://www.medworm.com/index.php?rid=5142213&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21536497%26dopt%3DAbstract</link>
            <description>This study was performed to generate a protocol that improves development and quality of humanized mice in the BALB/c-Rag2(null)Il2rγ(null) strain, testing route of injection, in vitro culture and freezing of hHSCs, types of cytokines in the culture, and co-injection of lineage-depleted CD34(-) cells. Specific hHSC culturing conditions and the addition of support cells were found to increase the frequency, and human hematopoietic chimerism, of humanized mice. The optimized protocol resulted in BALB/c-Rag2(null)Il2rγ(null) humanized mice displaying more consistent human hematopoietic and lymphoid engraftment. Thus, hematopoietic humanized mice generated on a BALB/c immunodeficient background represent a useful model to study the human immune system.
    PMID: 21536497 [PubMed - indexed fo...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5142213</comments>
            <pubDate>Thu, 30 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5142213</guid>        </item>
        <item>
            <title>Dalfampridine in multiple sclerosis: From symptomatic treatment to immunomodulation.</title>
            <link>http://www.medworm.com/index.php?rid=5062722&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21742559%26dopt%3DAbstract</link>
            <description>Authors: Espejo C, Montalban X
    Multiple sclerosis (MS) is a neurodegenerative disease that is deemed to affect more than 2.1 million people worldwide, and for which there is no cure. Early symptoms of MS are believed to result from axonal demyelination leading to slowing or blockade of impulse conduction. The blockade of K+ channels has been proven to improve conduction deficiencies secondary to demyelination in patients with MS. Dalfampridine is a K+ channel blocker that was recently approved by FDA for the symptomatic treatment of ambulation hardship in MS. Understanding the mechanisms by which Dalfampridine exerts its therapeutic effects is a complex issue as it blocks a wide variety of K+ channels that are distributed across multiple cell types in the nervous system but also in the...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5062722</comments>
            <pubDate>Fri, 24 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5062722</guid>        </item>
        <item>
            <title>Autoantibodies to villin occur frequently in IPEX, a severe immune dysregulation, syndrome caused by mutation of FOXP3.</title>
            <link>http://www.medworm.com/index.php?rid=5062723&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21741320%26dopt%3DAbstract</link>
            <description>Authors: Kobayashi I, Kubota M, Yamada M, Tanaka H, Itoh S, Sasahara Y, Whitesell L, Ariga T
    Intractable diarrhea is a major symptom of immune dysregulation, polyendocrinopathy, enteropathy, X-linked (IPEX) syndrome and associated with autoantibodies against enterocytes. Although autoimmune enteropathy (AIE)-related 75kDa antigen (AIE-75) is a prominent autoantigen involved in the enteropathy associated with IPEX syndrome, some patients with this syndrome demonstrated autoantibody recognizing a 95kDa protein rather than AIE-75 in the small intestine. We, herewith, identified villin, an actin-binding protein, as the 95kDa antigen. Four of five sera from patients with IPEX syndrome reacted with a fusion protein of glutathione-S-transferase and full length villin (GST-villin), whereas onl...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5062723</comments>
            <pubDate>Sun, 12 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5062723</guid>        </item>
        <item>
            <title>Cladribine as a therapeutic option in multiple sclerosis.</title>
            <link>http://www.medworm.com/index.php?rid=5011329&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21733757%26dopt%3DAbstract</link>
            <description>Authors: Warnke C, Leussink VI, Goebels N, Aktas O, Boyko A, Kieseier BC, Hartung HP
    There is an unmet need for more potent and convenient drugs in the treatment of patients diagnosed with multiple sclerosis (MS). Among five currently investigated oral drugs with an ongoing or completed phase III program, promising efficacy data for oral cladribine have recently been published. However, benefits need to be weighed against potential risks to define the role of this compound within current treatment regimens. Here we review present data on efficacy of oral cladribine and discuss known and anticipated risks of this drug.
    PMID: 21733757 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5011329</comments>
            <pubDate>Tue, 31 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5011329</guid>        </item>
        <item>
            <title>Clinical and immunological manifestations of patients with atypical severe combined immunodeficiency.</title>
            <link>http://www.medworm.com/index.php?rid=4963081&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21664875%26dopt%3DAbstract</link>
            <description>We report 10 new patients with such &quot;atypical&quot; SCID and summarize 63 patients from the literature. The patient groups with T(low)B(low) (n=28), T(low)B(+) (n=16) and ADA (n=29) SCID variants had similar infection profiles but differed in the frequency of immune dysregulation, which was observed predominantly in patients with recombination defects. Most immunological parameters were remarkably similar in the three groups. Of note, 19/68 patients with &quot;atypical&quot; SCID had normal T cell counts, 48/68 had normal IgG and 23/46 had at least one normal specific antibody titer. Elevated IgE was a characteristic feature of ADA deficiency. This overview characterizes &quot;atypical&quot; SCID as a distinct disease with immune dysregulation in addition to infection susceptibility. Lymphopenia, reduced naïve T ...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4963081</comments>
            <pubDate>Sun, 29 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4963081</guid>        </item>
        <item>
            <title>Fingolimod in multiple sclerosis: Mechanisms of action and clinical efficacy.</title>
            <link>http://www.medworm.com/index.php?rid=4963080&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21669553%26dopt%3DAbstract</link>
            <description>Authors: Ingwersen J, Aktas O, Kuery P, Kieseier B, Boyko A, Hartung HP
    Fingolimod, also known as FTY720, has recently been approved by the regulatory authorities in the US, EU, Australia, Russia, among others, for the treatment of relapsing-remitting multiple sclerosis. Fingolimod therefore represents the first oral drug for the treatment of this autoimmune disease of the central nervous system. Fingolimod modulates sphingosine-1 phosphate receptors and has unique immunoregulatory properties. Mechanistic studies from animal models have shown that fingolimod prevents immune cells from exiting from the lymphoid tissue and reaching the inflammatory tissue. Indeed, two phase III studies that laid the basis for fingolimod's approval demonstrated that fingolimod efficiently improves the rel...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4963080</comments>
            <pubDate>Wed, 25 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4963080</guid>        </item>
        <item>
            <title>Regulatory T cells as modulators of B cell antibody production.</title>
            <link>http://www.medworm.com/index.php?rid=4920849&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21652014%26dopt%3DAbstract</link>
            <description>Authors: Crispín JC
    
    PMID: 21652014 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4920849</comments>
            <pubDate>Mon, 23 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4920849</guid>        </item>
        <item>
            <title>Elevated plasma IL-22 levels correlated with Th1 and Th22 cells in patients with immune thrombocytopenia.</title>
            <link>http://www.medworm.com/index.php?rid=4920848&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21652269%26dopt%3DAbstract</link>
            <description>Authors: Cao J, Chen C, Zeng L, Li L, Li X, Li Z, Xu K
    
    PMID: 21652269 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4920848</comments>
            <pubDate>Thu, 19 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4920848</guid>        </item>
        <item>
            <title>Lack of increased prevalence of immunoregulatory disorders in hereditary angioedema due to C1-inhibitor deficiency.</title>
            <link>http://www.medworm.com/index.php?rid=4920851&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21636327%26dopt%3DAbstract</link>
            <description>Authors: Farkas H, Csuka D, Gács J, Czaller I, Zotter Z, Füst G, Varga L, Gergely P
    Hereditary angioedema due to deficiency of C1-INH (HAE-C1-INH) is associated with enhanced consumption of the early complement components, which may predispose for autoimmune disease. We assessed the prevalence of such disorders among HAE- C1-INH patients and their impact on the natural course of HAE-C1-INH. Clinical data and immunoserological parameters of 130 HAE-C1-INH and 174 non-C1-INH-deficient patients with angioedema were analyzed. In our study, the incidence of immunoregulatory disorders was 11.5% in the population of HAE-C1-INH patients and 5.2% among non-C1-INH-deficient controls with angioedema. Immunoserology screening revealed a greater prevalence of anticardiolipin IgM (p=0.0118) among ...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4920851</comments>
            <pubDate>Wed, 18 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4920851</guid>        </item>
        <item>
            <title>Developing understanding of the roles of CD1d-restricted T cell subsets in cancer: Reversing tumor-induced defects.</title>
            <link>http://www.medworm.com/index.php?rid=4920850&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21646050%26dopt%3DAbstract</link>
            <description>Authors: Exley MA, Lynch L, Varghese B, Nowak M, Alatrakchi N, Balk SP
    Invariant natural killer T-cells ('iNKT') are the best-known CD1d-restricted T-cells, with recently-defined roles in controlling adaptive immunity. CD1d-restricted T-cells can rapidly produce large amounts of Th1 and/or Th2//Treg/Th17-type cytokines, thereby regulating immunity. iNKT can stimulate potent anti-tumor immune responses via production of Th1 cytokines, direct cytotoxicity, and activation of effectors. However, Th2//Treg-type iNKT can inhibit anti-tumor activity. Furthermore, iNKT are decreased and/or reversibly functionally impaired in many advanced cancers. In some cases, CD1d-restricted T-cell cancer defects can be traced to CD1d(+) tumor interactions, since hematopoietic, prostate, and some other tumo...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4920850</comments>
            <pubDate>Thu, 12 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4920850</guid>        </item>
        <item>
            <title>Simian immunodeficiency virus infection in rhesus macaques induces selective tissue specific B cell defects in double positive CD21+CD27+ memory B cells.</title>
            <link>http://www.medworm.com/index.php?rid=4920852&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21622026%26dopt%3DAbstract</link>
            <description>Authors: Das A, Veazey RS, Wang X, Lackner AA, Xu H, Pahar B
    B cell dysfunction represents a central feature in HIV infection and pathogenesis. Our recent studies have shown that peripheral and lymphoid double positive CD21+CD27+ B cells were able to become activated and proliferate at higher rates than other B cell subpopulations. Increased proliferation of tonsillar memory B cells was identified compared to other tissues examined. Here, we demonstrate the decreased proliferation of tonsillar memory (CD21+CD27+) B cells during acute SIV infection also suggests that these cells may play an important role in SIV pathogenesis. Our findings demonstrate that SIV infection may induce selective defective responses in specific tissues, by suppressing memory B cell proliferation in tissues.
  ...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4920852</comments>
            <pubDate>Wed, 11 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4920852</guid>        </item>
        <item>
            <title>Protein transduction for tolerance induction.</title>
            <link>http://www.medworm.com/index.php?rid=4871422&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21600852%26dopt%3DAbstract</link>
            <description>Authors: Rogers GL, Herzog RW
    
    PMID: 21600852 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4871422</comments>
            <pubDate>Sat, 07 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4871422</guid>        </item>
        <item>
            <title>Expanded subpopulation of FoxP3(+) T regulatory cells in renal cell carcinoma co-express Helios, indicating they could be derived from natural but not induced Tregs.</title>
            <link>http://www.medworm.com/index.php?rid=4871426&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21570917%26dopt%3DAbstract</link>
            <description>Authors: Elkord E, Sharma S, Burt DJ, Hawkins RE
    Conversion of conventional T cells into T regulatory cells (Tregs) has been proposed as a potential mechanism for Treg expansion in cancer. However, this evidence is supported by in vitro or mouse model studies with no data from in vivo or human studies to support its role in enriching peripheral and tumor-infiltrating Tregs. Recent work has shown that induced FoxP3(+) Tregs (iTregs) do not express Helios; an Ikaros family transcription factor. We analyzed peripheral blood samples from untreated renal cell carcinoma (RCC) patients and following interleukin (IL)-2 treatment for the expression of FoxP3 and Helios. Our work shows that expanded peripheral FoxP3(+) Tregs in untreated RCC patients co-express Helios. Interestingly, IL-2 adminis...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4871426</comments>
            <pubDate>Thu, 28 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4871426</guid>        </item>
        <item>
            <title>Measuring adrenal autoantibody response: Interlaboratory concordance in the first international serum exchange for the determination of 21-hydroxylase autoantibodies.</title>
            <link>http://www.medworm.com/index.php?rid=4871427&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21570358%26dopt%3DAbstract</link>
            <description>Authors: Falorni A, Chen S, Zanchetta R, Yu L, Tiberti C, Bacosi ML, Furmaniak J, Bini V, Dotta F, Eisenbarth GS, Rees Smith B, Betterle C
    21-hydroxylase autoantibodies (21OHAb) are the gold standard immune marker to identify patients with clinical or subclinical autoimmune Addison's disease (AAD). No assessment of interlaboratory concordance has been made for 21OHAb measurement. Serum samples from 267 patients with primary adrenal insufficiency and from 83 healthy control subjects were distributed to four independent laboratories that determined presence and titer of 21OHAb, by using radiobinding assays with either in vitro translated (35)S-radiolabelled or (125)I-radiolabelled autoantigen. Cohen's κ of inter-rater agreement ranged from 0.857 to 0.983, showing a very good concordance...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4871427</comments>
            <pubDate>Wed, 27 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4871427</guid>        </item>
        <item>
            <title>Activation of the receptor for advanced glycation end products (RAGE) exacerbates experimental autoimmune myasthenia gravis symptoms.</title>
            <link>http://www.medworm.com/index.php?rid=4871425&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21570918%26dopt%3DAbstract</link>
            <description>Authors: Mu L, Zhang Y, Sun B, Wang J, Xie X, Li N, Zhang J, Kong Q, Liu Y, Han Z, Wang G, Fu Z, Yu B, Li G, Li H
    RAGE belongs to immunoglobulin superfamily and serves as a ligand for various immunoregulatory molecules including S100B that has been demonstrated important to T cell mediated autoimmune diseases. In this context, we hypothesized that RAGE could also impact B cell mediated, T cell-dependent autoimmune diseases. This was tested using myasthenia gravis (MG) animal model, EAMG. We show that expression of both RAGE and S100B are increased during EAMG and the interaction between RAGE and S100B affected the Th1/Th2/Th17/Treg cell equilibrium, up-regulate AChR-specific T cell proliferation. Furthermore, addition of S100B in vitro stimulated splenocyte activity linked to COX-2 up-...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4871425</comments>
            <pubDate>Wed, 27 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4871425</guid>        </item>
        <item>
            <title>NKT-cell-based immunotherapies in clinical trials.</title>
            <link>http://www.medworm.com/index.php?rid=4871423&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21592864%26dopt%3DAbstract</link>
            <description>Authors: Exley MA, Nakayama T
    
    PMID: 21592864 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4871423</comments>
            <pubDate>Wed, 27 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4871423</guid>        </item>
        <item>
            <title>The role of interferon alpha in initiation of type I diabetes in the NOD mouse.</title>
            <link>http://www.medworm.com/index.php?rid=4871424&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21592863%26dopt%3DAbstract</link>
            <description>Authors: Li Q, McDevitt HO
    Type 1 diabetes (T1D) is an autoimmune disease in both humans and the nonobese diabetic (NOD) mouse, in which the insulin-producing-cells of the pancreatic islets are destroyed by a beta islet cell-specific T cell immune response. We recently reported that interferon (IFN)-α is an early trigger of the T1D process in NOD mice. Here, we show that extensive blockade of IFN-α action by a monoclonal antibody specific to IFN-α receptor 1 results in nearly complete prevention of T1D in NOD mice. Whether professional IFN-α producing cells, plasmacytoid dendritic cells (pDCs), are responsible for the initiation of T1D has been unclear. Here we demonstrate that depletion of pDCs in NOD mice by a specific mAb given at 15-25days of age significantly delays the onset ...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4871424</comments>
            <pubDate>Thu, 21 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4871424</guid>        </item>
        <item>
            <title>B cells &quot;transduced&quot; with TAT-fusion proteins can induce tolerance and protect mice from diabetes and EAE.</title>
            <link>http://www.medworm.com/index.php?rid=4815761&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21546313%26dopt%3DAbstract</link>
            <description>B cells &quot;transduced&quot; with TAT-fusion proteins can induce tolerance and protect mice from diabetes and EAE.
    Clin Immunol. 2011 Apr 20;
    Authors: Su Y, Zhang AH, Li X, Owusu-Boaitey N, Skupsky J, Scott DW
    Antigen-immunoglobulin fusion protein expressing B cells have been shown as excellent tolerogenic antigen-presenting cells in multiple disease models. Using efficient protein transduction by fusion with a HIV TAT protein transduction domain, we herein tested the TAT-fusion protein transduced B cells for their effects in antigen-specific tolerance induction in two animal models, experimental autoimmune encephalomyelitis (EAE) and type 1 diabetes. We demonstrated that transfer of TAT-MOG(35-55) (myelin oligodendrocyte glycoprotein)-Ig 'transduced B cells' 10days after EAE induction...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4815761</comments>
            <pubDate>Tue, 19 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4815761</guid>        </item>
        <item>
            <title>Carbohydrate-binding motif in chitinase 3-like 1 (CHI3L1/YKL-40) specifically activates Akt signaling pathway in colonic epithelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=4815760&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21546314%26dopt%3DAbstract</link>
            <description>In conclusion, CBM region of CHI3L1 is critical in activating Akt signaling in CECs, and the activation may be associated with the development of chronic colitis.
    PMID: 21546314 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4815760</comments>
            <pubDate>Tue, 19 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4815760</guid>        </item>
        <item>
            <title>Induction of type B synoviocyte-like cells from plasmacytoid dendritic cells of the bone marrow in rheumatoid arthritis and osteoarthritis.</title>
            <link>http://www.medworm.com/index.php?rid=4815759&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21550856%26dopt%3DAbstract</link>
            <description>We examined the capacities of bone marrow (BM) plasmacytoid dendritic cells (pDC) to differentiate into type B synoviocyte-like cells. BM aspiration samples were obtained from 24 rheumatoid arthritis (RA) patients and 19 osteoarthritis (OA) patients during joint operations from the iliac crest. CD34+ cells and pDC purified from BM mononuclear cells were cultured with or without SCF, GM-CSF, and TNF-α for 2-4weeks. RA BM pDC as well as OA BM pDC comparably differentiated into fibroblast-like cells (FLC), expressing cadherin-11 and producing MMP-1, especially in the presence of TNF-α. Of note, depletion of BDCA4+ pDC from RA BM CD34+ cells significantly diminished their capacities to differentiate into FLC, which were restored by addition of BDCA4+cells in a dose-response manner. These res...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4815759</comments>
            <pubDate>Tue, 19 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4815759</guid>        </item>
        <item>
            <title>Immune mechanisms of new therapeutic strategies in multiple sclerosis-A focus on alemtuzumab.</title>
            <link>http://www.medworm.com/index.php?rid=4815758&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21550857%26dopt%3DAbstract</link>
            <description>Authors: Klotz L, Meuth SG, Wiendl H
    Alemtuzumab is a humanized monoclonal antibody targeting CD52, a broadly expressed cell surface molecule on immune cells. Application results in a rapid and long-lasting removal of lymphocyte populations from the circulation. Alemtuzumab-treatment of MS patients with relapsing-remitting forms of the disease significantly reduced the risk of relapse and accumulation of disability compared to interferon β-1a treatment in a phase II trial. Interestingly, further analysis together with parallel experimental studies suggested that alemtuzumab not only reduces disease activity due to its immune cell-depleting effect, but also confers neuroprotective effects, presumably by inducing production of neurotrophic factors in autoreactive T cells. However, alemt...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4815758</comments>
            <pubDate>Thu, 14 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4815758</guid>        </item>
        <item>
            <title>Treatment of multiple sclerosis with Anti-CD20 antibodies.</title>
            <link>http://www.medworm.com/index.php?rid=4815757&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21555250%26dopt%3DAbstract</link>
            <description>Authors: Barun B, Bar-Or A
    The recently successful targeting of B cells in patients with multiple sclerosis (MS) using monoclonal antibodies (mAbs) targeting CD20 has established that it is no longer a question of whether B cells contribute, but how they contribute, to MS disease activity. Here, the focus will be to review results that have emerged over the last few years from clinical trials of different anti-CD20 mAbs in patients with MS. We will also consider the biological basis underlying the apparent therapeutic efficacy of B cell depletion in MS. To this end, we will draw on several instructive observations made in MS patients who were treated with the anti-CD20 mAb rituximab. While the initial application of rituximab to patients with MS was based on the concept that B cell dep...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4815757</comments>
            <pubDate>Thu, 14 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4815757</guid>        </item>
        <item>
            <title>Generation of hematopoietic humanized mice in the newborn BALB/c-Rag2(null)Il2rγ(null) mouse model: A multivariable optimization approach.</title>
            <link>http://www.medworm.com/index.php?rid=4815762&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21536497%26dopt%3DAbstract</link>
            <description>This study was performed to generate a protocol that improves development and quality of humanized mice in the BALB/c-Rag2(null)Il2rγ(null) strain, testing route of injection, in vitro culture and freezing of hHSCs, types of cytokines in the culture, and co-injection of lineage-depleted CD34(-) cells. Specific hHSC culturing conditions and the addition of support cells were found to increase the frequency, and human hematopoietic chimerism, of humanized mice. The optimized protocol resulted in BALB/c-Rag2(null)Il2rγ(null) humanized mice displaying more consistent human hematopoietic and lymphoid engraftment. Thus, hematopoietic humanized mice generated on a BALB/c immunodeficient background represent a useful model to study the human immune system.
    PMID: 21536497 [PubMed - as supplie...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4815762</comments>
            <pubDate>Wed, 13 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4815762</guid>        </item>
        <item>
            <title>Early versus delayed diagnosis of SCID: Triumph versus tragedy.</title>
            <link>http://www.medworm.com/index.php?rid=4815766&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21497138%26dopt%3DAbstract</link>
            <description>Authors: Nicholas S, Krance RA, Hanson IC, Chinen J, Mamlok RJ, Roifman CM, Shearer WT
    
    PMID: 21497138 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4815766</comments>
            <pubDate>Tue, 12 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4815766</guid>        </item>
        <item>
            <title>The number of circulating CD4(+)CD25(high)Foxp3(+) T lymphocytes is transiently elevated in the early childhood of transient hypogammaglobulinemia of infancy patients.</title>
            <link>http://www.medworm.com/index.php?rid=4815763&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21531630%26dopt%3DAbstract</link>
            <description>Authors: Rutkowska M, Lenart M, Bukowska-Strakovà K, Szaflarska A, Pituch-Noworolska A, Kobylarz K, Błaut-Szlósarczyk A, Zwonarz K, Zembala M, Siedlar M
    
    PMID: 21531630 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4815763</comments>
            <pubDate>Tue, 12 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4815763</guid>        </item>
        <item>
            <title>Activation of human invariant natural killer T cells with a thioglycoside analogue of α-galactosylceramide.</title>
            <link>http://www.medworm.com/index.php?rid=4815767&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21493160%26dopt%3DAbstract</link>
            <description>Authors: Hogan AE, O'Reilly V, Dunne MR, Dere RT, Zeng SG, O'Brien C, Amu S, Fallon PG, Exley MA, O'Farrelly C, Zhu X, Doherty DG
    Activation of CD1d-restricted invariant NKT (iNKT) cells with the glycolipid α-galactosylceramide (α-GalCer) confers protection against disease in murine models, however, clinical trials in humans have had limited impact. We synthesized a novel thioglycoside analogue of α-GalCer, denoted α-S-GalCer, and tested its efficacy for stimulating human iNKT cells in vitro. α-S-GalCer stimulated cytokine release by iNKT cells in a CD1d-dependent manner and primed CD1d(+) target cells for lysis. α-S-GalCer-stimulated iNKT cells induced maturation of monocyte-derived dendritic cells into antigen-presenting cells that released IL-12 and small amounts of IL-10. The...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4815767</comments>
            <pubDate>Mon, 11 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4815767</guid>        </item>
        <item>
            <title>Age-associated alteration in naive and memory Th17 cell response in humans.</title>
            <link>http://www.medworm.com/index.php?rid=4815769&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21489886%26dopt%3DAbstract</link>
            <description>Authors: Lee JS, Lee WW, Kim SH, Kang Y, Lee N, Shin MS, Kang SW, Kang I
    Th17 cells produce IL-17 that plays an important role in host defense. However, little is known about whether aging affects human Th17 cells. Here we demonstrated that healthy elderly people (age≥65) had a decreased frequency of IL-17-producing cells in memory CD4(+) T cells compared to healthy young people (age≤40) while both groups had similar frequencies of IFN-γ-producing cells in the same memory cell subset as measured by flow cytometry. In contrast, the healthy elderly had increased differentiation of IL-17-producing effector cells but not IFN-γ-producing cells from naive CD4(+) T cells compared to the healthy young. The results of ELISA also showed similar findings with increased IL-17 production from...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4815769</comments>
            <pubDate>Sun, 10 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4815769</guid>        </item>
        <item>
            <title>Myelin-reactive antibodies mediate the pathology of MBP-PLP fusion protein MP4-induced EAE.</title>
            <link>http://www.medworm.com/index.php?rid=4815768&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21489887%26dopt%3DAbstract</link>
            <description>Authors: Kuerten S, Pauly R, Rottlaender A, Rodi M, Gruppe TL, Addicks K, Tary-Lehmann M, Lehmann PV
    Experimental autoimmune encephalomyelitis (EAE) is frequently used for studies of multiple sclerosis (MS). Because in most EAE models T cells mediate the pathology in the absence of B cells/autoantibodies, the notion has evolved that also MS may be a primarily T cell-mediated disease. We have previously introduced MBP-PLP fusion protein (MP4)-induced EAE in C57BL/6 mice. Here we show that the disease in this model is antibody-dependent. Immunization of B cell-deficient mice did not induce EAE. When such B cell-deficient mice were, however, injected with MBP/PLP-specific antibodies in addition to the immunization with MP4, they developed disease of a severity and course that was similar ...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4815768</comments>
            <pubDate>Sun, 10 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4815768</guid>        </item>
        <item>
            <title>Regulatory T cells with reduced repressor capacities are extensively amplified in pulmonary sarcoid lesions and sustain granuloma formation.</title>
            <link>http://www.medworm.com/index.php?rid=4815770&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21482483%26dopt%3DAbstract</link>
            <description>Authors: Rappl G, Pabst S, Riemann D, Schmidt A, Wickenhauser C, Schütte W, Hombach AA, Seliger B, Grohé C, Abken H
    Sarcoidosis can evolve into a chronic disease with persistent granulomas accompanied by progressive fibrosis. While an unlimited inflammatory response suggests an impaired immune control in sarcoid lesions, it stands in contrast to the massive infiltration with CD4(+)CD25(high)FoxP3(+) regulatory T cells. We here revealed that those Treg cells in affected lung lesions were mainly derived from activated natural Treg cells with GARP (LRRC32)-positive phenotype but exhibited reduced repressor capacities despite high IL-10 and TGF-beta 1 levels. The repressive capacity of blood Treg cells, in contrast, was not impaired compared to age-matched healthy donors. Treg derived ce...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4815770</comments>
            <pubDate>Fri, 08 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4815770</guid>        </item>
        <item>
            <title>Mast cells and tumour necrosis factor alpha (TNF-α): Partners in crime in asthma pathogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=4815764&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21514238%26dopt%3DAbstract</link>
            <description>Authors: Oettgen HC
    
    PMID: 21514238 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4815764</comments>
            <pubDate>Wed, 06 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4815764</guid>        </item>
        <item>
            <title>IL-10-conditioned dendritic cells prevent autoimmune diabetes in NOD and humanized HLA-DQ8/RIP-B7.1 mice.</title>
            <link>http://www.medworm.com/index.php?rid=4815771&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21458378%26dopt%3DAbstract</link>
            <description>This study was to determine whether BMDCs cultured in the presence of IL-10 (G/10-DCs) could promote T cell tolerance and prevent autoimmune diabetes in two different animal models of T1D. Our results showed that G/10-DCs suppressed both insulitis and spontaneous diabetes in NOD and HLA-DQ8/RIP-B7.1 mice. The suppression was likely to be mediated by T cells, as we found that regulatory CD4(+)CD25(+)Foxp3(+) cells were significantly increased in G/10-DC treated animals. In vivo, the G/10-DCs inhibited diabetogenic T cell proliferation; in vitro, they had reduced expression of costimulatory molecules and produced little IL-12/23 p40 or IL-6 but a large amount of IL-10 when compared with DCs matured in the presence of IL-4 (G/4-DC). We conclude that IL-10-treated DCs are tolerogenic and induc...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4815771</comments>
            <pubDate>Tue, 29 Mar 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4815771</guid>        </item>
        <item>
            <title>Galectin-9 administration ameliorates CVB3 induced myocarditis by promoting the proliferation of regulatory T cells and alternatively activated Th2 cells.</title>
            <link>http://www.medworm.com/index.php?rid=4815765&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21507728%26dopt%3DAbstract</link>
            <description>In this study we explored the effects of galectin-9 on CVB3 induced myocarditis and its possible mechanisms involved. We demonstrated that galectin-9 expression was significantly up-regulated in the myocardium following CVB3 infection and was correlated with the severity of viral myocarditis. To explore whether galectin-9 may have therapeutic effect on the CVB3 induced myocarditis, galectin-9 was administered daily to mice following CVB3 infection. Significantly reduced CD4(+) T cells and remarkably increased regulatory T cells frequency in the heart tissue were found as compared to the non-treated mice. It was accompanied by a significant decreased level of Th1 cytokines as TNF-α and IFN-γ both in the myocardium and serum, and an increased level of Th2 cytokines such as IL-4 and IL-10. ...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4815765</comments>
            <pubDate>Sun, 27 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4815765</guid>        </item>
        <item>
            <title>Th17 and Foxp3(+) T regulatory cell dynamics and distribution in myelodysplastic syndromes.</title>
            <link>http://www.medworm.com/index.php?rid=4655253&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21444247%26dopt%3DAbstract</link>
            <description>Authors: Bouchliou I, Miltiades P, Nakou E, Spanoudakis E, Goutzouvelidis A, Vakalopoulou S, Garypidou V, Kotoula V, Bourikas G, Tsatalas C, Kotsianidis I
    Foxp3(+) T regulatory cells (Tregs) and Th17 cells accumulate synchronously at tumor sites during cancer progression, where their interplay is apparently affecting the efficiency of the antitumor response. In myelodysplastic syndromes, a hematopoietic malignancy of myeloid origin, Tregs are highly increased in the late stages of the disease (L-MDS), but the mechanisms driving Treg expansion and the interaction between Treg and Th17 cell dynamics are still unknown. We demonstrate that the proliferative capacity of Tregs is deficient during the early MDS stages (E-MDS), while in L-MDS it returns to normal levels. In addition, synchrono...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4655253</comments>
            <pubDate>Sat, 26 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4655253</guid>        </item>
        <item>
            <title>Oxidized LDL immune complexes stimulate collagen IV production in mesangial cells via Fc gamma receptors I and III.</title>
            <link>http://www.medworm.com/index.php?rid=4655254&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21439910%26dopt%3DAbstract</link>
            <description>In this study, we have studied the effect of oxLDL-IC on collagen IV expression by mesangial cells. We found that oxLDL-IC markedly stimulated collagen IV expression in a concentration- and time-dependent fashion while oxLDL only had moderate effect. We also found that oxLDL-IC stimulated collagen IV expression by engaging Fc gamma receptor (FcγR) I and III, but not FcγRII, and that p38 MAPK, JNK and PKC pathways were involved in collagen IV expression. Furthermore, we found that oxLDL-IC stimulated FcγRI expression, suggesting a positive feedback mechanism involved in oxLDL-IC-stimulated collagen IV expression. Taken together, this study showed that oxLDL-IC stimulated collagen IV in mesangial cells via FcγRI and FcγRIII, and the expression of FcγRI was increased by oxLDL-IC.
    PM...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4655254</comments>
            <pubDate>Wed, 23 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4655254</guid>        </item>
        <item>
            <title>Targeting iNKT cells for the treatment of sickle cell disease.</title>
            <link>http://www.medworm.com/index.php?rid=4655255&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21429807%26dopt%3DAbstract</link>
            <description>Authors: Field JJ, Nathan DG, Linden J
    Sickle cell disease (SCD) causes widely disseminated vaso-occlusive episodes. Building on evidence implicating invariant NKT (iNKT) cells in the pathogenesis of ischemia/reperfusion injury, recent studies demonstrate that blockade of iNKT cell activation in mice with SCD reduces pulmonary inflammation and injury. In patients with SCD, iNKT cells in blood are increased in absolute number and activated in comparison to healthy controls. iNKT cell activation is reduced by agonists of adenosine 2A receptors (A(2A)Rs) such as the clinically approved coronary vasodilator, regadenoson. An ongoing multi-center, dose-finding and safety trial of infused regadenoson, has been initiated and is providing preliminary data about its safety and efficacy to treat ...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4655255</comments>
            <pubDate>Mon, 21 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4655255</guid>        </item>
        <item>
            <title>Neuroprotective agents: Cannabinoids.</title>
            <link>http://www.medworm.com/index.php?rid=4655256&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21420365%26dopt%3DAbstract</link>
            <description>Authors: Sánchez AJ, García-Merino A
    Chronic inflammation and neurodegeneration are the main pathological traits of multiple sclerosis that coexist in all stages of the disease course, with complex and still nonclarified relationships. Currently licensed medications have efficacy to control aspects related to inflammation, but have been unable to modify pure progression. Experimental work has provided robust evidence of the immunomodulatory and neuroprotective properties that cannabinoids exert in animal models of multiple sclerosis. Through activation of the CB2 receptor, cannabinoids modulate peripheral blood lymphocytes, interfere with migration across the blood-brain barrier and control microglial/macrophage activation. CB1 receptors present in neural cells have a fundamental rol...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4655256</comments>
            <pubDate>Thu, 17 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4655256</guid>        </item>
        <item>
            <title>Abrogation of pathogenic IgG autoantibody production in CD40L gene-deleted lupus-prone New Zealand Black mice.</title>
            <link>http://www.medworm.com/index.php?rid=4655258&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21414847%26dopt%3DAbstract</link>
            <description>Authors: Pau E, Chang NH, Loh C, Lajoie G, Wither JE
    New Zealand Black (NZB) mice spontaneously develop a lupus-like autoimmune disease. Since CD40-CD40L interactions are important for B cell class-switch recombination and germinal center formation, we sought to understand the impact of these interactions on the immune abnormalities in NZB CD40L gene-deleted (CD40L(-/-)) mice in vivo. NZB.CD40L(-/-) mice demonstrated abrogation of all IgG autoantibodies tested and attenuated kidney disease. However, polyclonal B cell activation in vivo and B cell proliferation and class-switching in response to TLR ligands in vitro were preserved in the absence of CD40L in NZB mice. Although, plasmacytoid dendritic cell expansion and elevated BAFF production were unaffected by the absence of CD40L, the...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4655258</comments>
            <pubDate>Tue, 15 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4655258</guid>        </item>
        <item>
            <title>Costimulatory signals potently modulate the T cell inhibitory capacity of the therapeutic CD11a antibody Efalizumab.</title>
            <link>http://www.medworm.com/index.php?rid=4655257&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21414849%26dopt%3DAbstract</link>
            <description>Authors: Kuschei WM, Leitner J, Majdic O, Pickl WF, Zlabinger GJ, Grabmeier-Pfistershammer K, Steinberger P
    The therapeutic CD11a antibody Efalizumab interferes with psoriasis pathogenesis by blocking T cell activation and migration. We have performed a detailed analysis on its effects during the activation of human T cells and found that the capability of Efalizumab to inhibit proliferation and cytokine production of T cells critically depends on the quality and quantity of costimulatory signals. Efalizumab potently inhibited the proliferation and cytokine production of human T cells costimulated via ICOS, OX40, CD27 or 4-1BB, but did not significantly inhibit T cells that received stimuli via CD2 or CD28. The capacity of CD2 and CD28 signals to interfere with the T cell inhibitory ef...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4655257</comments>
            <pubDate>Tue, 15 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4655257</guid>        </item>
        <item>
            <title>Intravenous immunoglobulin modulates the maturation of TLR 4-primed peripheral blood monocytes.</title>
            <link>http://www.medworm.com/index.php?rid=4655259&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21406333%26dopt%3DAbstract</link>
            <description>Authors: Ballow M, Allen C
    Intravenous immunoglobulin (IgIV) has immune modulating effects on the differentiation and function of dendritic cells (DC). Peripheral blood CD14+ monocytes were induced to differentiate into immature DC with IL-4/GM-CSF. DC maturation was analyzed by flow cytometry, and function assessed for antigen uptake and antigen processing. IgIV added during the differentiation process induced immature DC to differentiate into a mature DC with increased expression of CD83 and CCR7. A &quot;priming&quot; step with low concentrations of LPS or other TLR agonists that utilize the myD88 signaling pathway was necessary to observe these changes. These modulated DCs had reduced antigen uptake, but exhibited increased antigen presentation. Treatment of the IgIV with pepsin to generate ...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4655259</comments>
            <pubDate>Mon, 14 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4655259</guid>        </item>
        <item>
            <title>A case of lichenoid drug eruption associated with subcutaneous immunoglobulin therapy.</title>
            <link>http://www.medworm.com/index.php?rid=4655260&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21402497%26dopt%3DAbstract</link>
            <description>Authors: Beccastrini E, Emmi G, Caproni M, Antiga E, Francalanci S, Lorenzoni A, Emmi L
    
    PMID: 21402497 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4655260</comments>
            <pubDate>Sat, 12 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4655260</guid>        </item>
        <item>
            <title>Repressor of GATA negatively regulates murine contact hypersensitivity through the inhibition of type-2 allergic responses.</title>
            <link>http://www.medworm.com/index.php?rid=4593076&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21398189%26dopt%3DAbstract</link>
            <description>Authors: Hirasaki Y, Iwamura C, Yamashita M, Ito T, Kitajima M, Shinoda K, Namiki T, Terasawa K, Nakayama T
    Repressor of GATA (ROG) inhibits Th2 cell differentiation and allergic airway inflammation in the lung. To determine the role of ROG in the pathogenesis of contact hypersensitivity (CHS), a hapten-induced mouse model of CHS using ROG Tg and ROG-deficient (ROG(-/-)) was used. ROG Tg mice showed little ear swelling, while ROG(-/-) mice showed enhanced ear swelling in comparison to wild type mice. Interstitial edema and mast cell degranulation at the local inflammation sites were mild in ROG Tg mice and exacerbated in ROG(-/-) mice. In addition, the serum total IgE and hapten-specific IgG1 levels were increased in ROG(-/-) mice. Adoptive transfer of ROG(-/-) CD4(+) T cells exacerbat...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4593076</comments>
            <pubDate>Fri, 11 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4593076</guid>        </item>
        <item>
            <title>Antigen-specific IgA B memory cell responses to Shigella antigens elicited in volunteers immunized with live attenuated Shigella flexneri 2a oral vaccine candidates.</title>
            <link>http://www.medworm.com/index.php?rid=4593078&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21388888%26dopt%3DAbstract</link>
            <description>Authors: Simon JK, Maciel M, Weld ED, Wahid R, Pasetti MF, Picking WL, Kotloff KL, Levine MM, Sztein MB
    We studied the induction of antigen-specific IgA memory B cells (B(M)) in volunteers who received live attenuated Shigella flexneri 2a vaccines. Subjects ingested a single oral dose of 10(7), 10(8) or 10(9) CFU of S. flexneri 2a with deletions in guaBA (CVD 1204) or in guaBA, set and sen (CVD 1208). Antigen-specific serum and stool antibody responses to LPS and Ipa B were measured on days 0, 7, 14, 28 and 42. IgA B(M) cells specific to LPS, Ipa B and total IgA were assessed on days 0 and 28. We show the induction of significant LPS-specific IgA B(M) cells in anti-LPS IgA seroresponders. Positive correlations were found between anti-LPS IgA B(M) cells and anti-LPS IgA in serum and sto...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4593078</comments>
            <pubDate>Mon, 07 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4593078</guid>        </item>
        <item>
            <title>Long-term non-progressors display a greater number of Th17 cells than HIV-infected typical progressors.</title>
            <link>http://www.medworm.com/index.php?rid=4593079&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21367666%26dopt%3DAbstract</link>
            <description>Authors: Salgado M, Rallón NI, Rodés B, López M, Soriano V, Benito JM
    Interleukin 17 (IL17) secreting T (Th17) cells play a protective role against bacterial infections at mucosal surfaces. Recent reports show Th17 cells are depleted in the gut associated lymphoid tissue of HIV+ patients, but their role in HIV disease progression is not well understood. Expression of the IL17 receptor (IL17R) and the production of IL17 were compared between two groups of HIV patients with different disease progression (long-term-nonprogressors, LTNP and typical-progressors, TP). IL17R expression was similar in LTNP and TP, whereas Th17 cell number was greater in LTNP than TP (p=0.015). An inverse correlation between the plasma HIV-RNA and both IL17R expression and Th17 cell number was found (p=0.001...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4593079</comments>
            <pubDate>Tue, 01 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4593079</guid>        </item>
        <item>
            <title>Immune mechanisms of new therapeutic strategies in MS - Teriflunomide.</title>
            <link>http://www.medworm.com/index.php?rid=4593080&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21367665%26dopt%3DAbstract</link>
            <description>Authors: Claussen MC, Korn T
    At present, a series of oral disease-modifying agents is being introduced for the treatment of multiple sclerosis. With the exception of laquinimod, the &quot;new&quot; oral compounds have already been approved for other indications such as organ transplantation (FTY720), psoriasis (dimethylfumarate), hairy cell leukemia (cladribine), and rheumatoid arthritis (leflunomide). Leflunomide is the prodrug of teriflunomide which is the latest compound that has successfully been tested in a large phase III clinical trial in relapsing MS. Due to its favorable safety profile and its efficacy in rheumatoid arthritis where the aberrant immune response is in various aspects similar to the autoimmune reaction in MS patients, teriflunomide is a promising treatment option for MS pa...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4593080</comments>
            <pubDate>Mon, 28 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4593080</guid>        </item>
        <item>
            <title>Toll-like receptors 7 and 8 expression is associated with poor outcome and greater inflammatory response in acute ischemic stroke.</title>
            <link>http://www.medworm.com/index.php?rid=4593081&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21354862%26dopt%3DAbstract</link>
            <description>In conclusion, TLR 7 and TLR8 expressions are associated with poor outcome and greater inflammatory response in acute ischemic stroke.
    PMID: 21354862 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4593081</comments>
            <pubDate>Fri, 25 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4593081</guid>        </item>
        <item>
            <title>Interaction of HLA-DRB1*1501 allele and TNF-alpha -308 G/A single nucleotide polymorphism in the susceptibility to multiple sclerosis.</title>
            <link>http://www.medworm.com/index.php?rid=4593077&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21396892%26dopt%3DAbstract</link>
            <description>In this study, we have evaluated the impact of HLA-DRB1*1501 allele and TNF-alpha -308 G/A single nucleotide polymorphism, and their interaction, in the susceptibility to MS in Iranian population. Genomic DNA samples were prepared from whole blood of 366 MS Patients and 414 control subjects. The genotypes were determined by SSP-PCR method. Frequency of alleles and genotypes were compared between the two groups by using Fisher's exact test. HLA-DRB1*1501 allele was more frequent among patients (OR=1.57, P=0.0026). TNF-α -308 G allele and G/G genotype had higher frequency among MS patients than control subjects (G vs. A: OR=1.26, P&amp;lt;0.05); G/G vs. A/A: OR=4.59, P=0.0003). The odds ratio was higher among HLA-DRB1*1501 positive individuals. Co-existence of TNF G and HLA-DRB1*1501 alleles sh...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4593077</comments>
            <pubDate>Sat, 12 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4593077</guid>        </item>
        <item>
            <title>Primed status of transitional B cells associated with their presence in the cerebrospinal fluid in early phases of multiple sclerosis.</title>
            <link>http://www.medworm.com/index.php?rid=4479678&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21310664%26dopt%3DAbstract</link>
            <description>Authors: Lee-Chang C, Top I, Zéphir H, Dubucquoi S, Trauet J, Dussart P, Prin L, Vermersch P
    In the present study we showed that transitional B cells of patients with clinically isolated syndrome (CIS) and relapsing-remitting multiple sclerosis (RR-MS) are reduced in the peripheral blood (PB) (5.5- and 3.7-fold, respectively). In addition, these cells appeared to up-regulate different integrins (α4 and β1). These observations were associated with a primed cellular status, confirmed by an increased proportion of circulating CD80(+) transitional B cells. Interestingly, these results correlate with presence of transitional B cells in the CSF. Furthermore, these cells were absent in the CSF of individuals with other inflammatory neurological disease, and their levels in paired PB and CD...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4479678</comments>
            <pubDate>Tue, 08 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4479678</guid>        </item>
        <item>
            <title>Increase of regulatory T cells and the ratio of specific IgE to total IgE are candidates for response monitoring or prognostic biomarkers in 2-year sublingual immunotherapy (SLIT) for Japanese cedar pollinosis.</title>
            <link>http://www.medworm.com/index.php?rid=4479681&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21300571%26dopt%3DAbstract</link>
            <description>Authors: Fujimura T, Yonekura S, Horiguchi S, Taniguchi Y, Saito A, Yasueda H, Inamine A, Nakayama T, Takemori T, Taniguchi M, Sakaguchi M, Okamoto Y
    The aims of this study were to examine the therapeutic effects of sublingual immunotherapy (SLIT) and to identify potential biomarkers that would predict the therapeutic response in a randomized, double-blind, placebo-controlled clinical trial. The trial was carried out over two pollinosis seasons in 2007 and 2008. Carry-over therapeutic effects were analyzed in 2009. SLIT significantly ameliorated the symptoms of pollinosis during the 2008 and 2009 pollen seasons. Cry j 1-specific cytokine production in a subgroup of patients with mild disease in the SLIT group was significantly attenuated. The ratio of specific IgE to total IgE before t...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4479681</comments>
            <pubDate>Sat, 05 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4479681</guid>        </item>
        <item>
            <title>Antibody and markers of T-cell activation illuminate the pathogenesis of HCV immune restoration disease in HIV/HCV co-infected patients commencing ART.</title>
            <link>http://www.medworm.com/index.php?rid=4479683&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21296026%26dopt%3DAbstract</link>
            <description>Authors: Yunihastuti E, Lee S, Gani RA, Saraswati H, Sundaru H, Lesmana L, Sukmana N, Price P
    Some HIV/hepatitis C virus co-infected patients beginning ART experience Immune Restoration Disease (IRD) manifested as a rise in serum alanine transaminase. This was investigated in HIV/HCV co-infected individuals (n=50) commencing ART in Jakarta (Indonesia). Samples were collected at weeks 0, 4, 8, 12, 24 and at HCV IRD. Nine patients experienced HCV IRD (incidence=9.2 per 1000 person-weeks). These resolved without changing treatment. Markers of T-cell activation (sCD26, sCD30) and immune recruitment (CXCL10) increased in many HCV IRD cases, so T-cells may mediate HCV IRD. Total anti-HCV antibody (core, NS3, NS4) remained lower in HCV IRD cases, but levels of antibody to core were not lower ...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4479683</comments>
            <pubDate>Thu, 03 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4479683</guid>        </item>
        <item>
            <title>Clinical heterogeneity and diagnostic delay of autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy syndrome.</title>
            <link>http://www.medworm.com/index.php?rid=4479684&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21295522%26dopt%3DAbstract</link>
            <description>Authors: Mazza C, Buzi F, Ortolani F, Vitali A, Notarangelo LD, Weber G, Bacchetta R, Soresina A, Lougaris V, Greggio NA, Taddio A, Pasic S, de Vroede M, Pac M, Kilic SS, Ozden S, Rusconi R, Martino S, Capalbo D, Salerno M, Pignata C, Radetti G, Maggiore G, Plebani A, Notarangelo LD, Badolato R
    Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) is a rare autosomal recessive organ-specific autoimmune disorder that is characterized by a variable combination of (i) chronic mucocutaneous candidiasis, (ii) polyendocrinopathy and/or hepatitis and (iii) dystrophy of the dental enamel and nails. We analyzed the AIRE (autoimmune regulator) gene in subjects who presented any symptom that has been associated with APECED, including candidiasis and autoimmune endocrinopathy. We...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4479684</comments>
            <pubDate>Wed, 02 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4479684</guid>        </item>
        <item>
            <title>Peripheral blood galectin-1-expressing T and natural killer cells in normal pregnancy and preeclampsia.</title>
            <link>http://www.medworm.com/index.php?rid=4479685&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21292557%26dopt%3DAbstract</link>
            <description>Authors: Molvarec A, Blois SM, Stenczer B, Toldi G, Tirado-Gonzalez I, Ito M, Shima T, Yoneda S, Vásárhelyi B, Rigó J, Saito S
    The purpose of this study was to determine whether the proportion of galectin-1-expressing peripheral blood T and NK cells is altered in normal pregnancy and preeclampsia (PE). We also examined whether circulating levels of galectin-1 and anti-galectin-1 autoantibodies are affected in PE. Seventy preeclamptic patients, 75 healthy pregnant and 21 healthy non-pregnant women were involved in this study. Serum galectin-1 and anti-galectin-1 autoantibody levels were measured by ELISA. Intracellular galectin-1 expression of lymphocytes was determined with flow cytometry. Serum galectin-1 and anti-galectin-1 IgG levels did not differ significantly between the healt...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4479685</comments>
            <pubDate>Tue, 01 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4479685</guid>        </item>
        <item>
            <title>Evidence for a modulatory effect of IL-10 on both Th1 and Th2 cytokine production: The role of the environment.</title>
            <link>http://www.medworm.com/index.php?rid=4479697&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21285005%26dopt%3DAbstract</link>
            <description>The objective of the present study was to investigate the effect of poor living environmental conditions on mitogen-induced production of cytokines (Th1 and Th2) by peripheral blood leukocytes in children living in urban Brazil and investigate the role of IL-10 in modifying this effect. Our data showed that the proportion of children producing Th1 and Th2 cytokines was lower among those with poor living conditions and that this finding was stronger in children producing IL-10. These results provide a possible biologic explanation for the temporal trends of increasing risk of inflammatory diseases observed in populations living in affluent countries.
    PMID: 21285005 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4479697</comments>
            <pubDate>Mon, 31 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4479697</guid>        </item>
        <item>
            <title>Detectable expression of IL-35 in CD4(+) T cells from peripheral blood of chronic Hepatitis B patients.</title>
            <link>http://www.medworm.com/index.php?rid=4479688&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21285006%26dopt%3DAbstract</link>
            <description>In this study, we investigated whether IL-35 expression could be detected in CD4(+) T cells from peripheral blood of chronic Hepatitis B patients. Using both RT-PCR and immunoprecipitation plus Western blot analysis, we demonstrated that IL-35 expression could be detected in the CD4(+) T cells from peripheral blood of Chronic Hepatitis B patients.
    PMID: 21285006 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4479688</comments>
            <pubDate>Mon, 31 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4479688</guid>        </item>
        <item>
            <title>B lymphocytes are resistant to death receptor 5-induced apoptosis.</title>
            <link>http://www.medworm.com/index.php?rid=4479705&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21276756%26dopt%3DAbstract</link>
            <description>We examined DR5 expression and function on B lymphocytes from healthy controls subjects, SLE patients, and human tonsil. DR5 was expressed similarly on all B cell subpopulations, including resting and activated B cells. Expression of DR5 was equivalent on B cells from SLE patients and healthy subjects. Additionally, DR5 expression was unchanged after B lymphocyte stimulation. However, B cells were resistant to DR5-induced apoptosis, including after in vitro activation. No changes in subsets of B cells were observed in subjects of a trial of CS-1008, an agonist anti-DR5. While DR5 shows promise as a way to selectively eliminate tumor cells and activated synoviocytes, these data suggest DR5 alone cannot be used as a target to remove pathogenic SLE B cells.
    PMID: 21276756 [PubMed - as sup...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4479705</comments>
            <pubDate>Thu, 27 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4479705</guid>        </item>
        <item>
            <title>Evaluation of (131)I-anti-MIF mAb as a reporter for allograft rejection.</title>
            <link>http://www.medworm.com/index.php?rid=4414295&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21273133%26dopt%3DAbstract</link>
            <description>In this study, we evaluated whether (131)I-anti-MIF mAb could be an efficient imaging reporter for monitoring allorejection. (131)I-anti-MIF mAb or control (131)I-IgG was injected to skin allotransplantation mice and T/NT ratios were evaluated. The imaging changes of grafts were dynamically displayed by whole-body images. The results showed that up-regulation of MIF expression was found in allografts but not in isografts. During the whole progression of rejection, the T/NT ratio in the (131)I-anti-MIF mAb group was significantly higher than that in the (131)I-IgG group and markedly increased on the top of rejection. The graft-rejection could also be shown more clearly in the (131)I-anti-MIF mAb group by whole-body imaging. These results implied that (131)I-anti-MIF mAb may be a valid metho...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4414295</comments>
            <pubDate>Tue, 25 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4414295</guid>        </item>
        <item>
            <title>Parameters of the classical complement pathway predict disease severity in hereditary angioedema.</title>
            <link>http://www.medworm.com/index.php?rid=4479682&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21300570%26dopt%3DAbstract</link>
            <description>Authors: Csuka D, Füst G, Farkas H, Varga L
    Functional C1-inhibitor (C1-inh) and C4 are potential severity markers of hereditary angioedema due to deficiency of C1-inh (HAE-C1-inh), and the complexes generated through complement activation may be relevant. We studied the association between disease severity and complement parameters in 105 HAE-C1-inh patients. Disease severity was characterized by the number of angioedema attacks or alternatively, by the number of C1-inh concentrate ampoules (C1-inh-amp) used for the treatment of attacks. Median C1rC1sC1-inh level was higher (32.8 U/ml vs. 3.4 U/ml; p&amp;lt;0.0001) in patients, compared to controls. C1rC1sC1-inh and C1-inh strongly correlated with attack number and C1-inh-amp, both in the whole patient population and in the subgroup on d...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4479682</comments>
            <pubDate>Thu, 20 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4479682</guid>        </item>
        <item>
            <title>Regulation of acute graft-versus-host disease by human umbilical cord blood derived stromal cells in haploidentical stem cell transplantation in mice through very late activation antigen-4.</title>
            <link>http://www.medworm.com/index.php?rid=4479679&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21310663%26dopt%3DAbstract</link>
            <description>This study aimed to investigate the possible mechanism by in vitro co-cultured splenocytes of donor mice with hUCBDSCs and in haploidentical stem cell transplantation in mice with acute GVHD. Both hUCBDSCs and human bone marrow stromal cells (hBMSCs) elicited decreased lymphocyte expression of VLA-4, but this decrease was stronger with hUCBDSCs than with hBMSCs (p&amp;lt;0.05). Cotransplantation of bone marrow with hUCBDSCs significantly decreased the expression of VLA-4 compared with control mice (p&amp;lt;0.05). A significant reduction of VLA-4 labeling in the target organs of GVHD was evident in haploidentical mice cotransplanted with hUCBDSCs. Our study shows that hUCBDSCs may protect mouse recipients of haploidentical stem cell transplantation from aGVHD via downregulating the expression of V...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4479679</comments>
            <pubDate>Thu, 20 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4479679</guid>        </item>
        <item>
            <title>Preparations of intravenous immunoglobulins diminish the number and proinflammatory response of CD14(+)CD16(++) monocytes in common variable immunodeficiency (CVID) patients.</title>
            <link>http://www.medworm.com/index.php?rid=4479680&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21300572%26dopt%3DAbstract</link>
            <description>Authors: Siedlar M, Strach M, Bukowska-Strakova K, Lenart M, Szaflarska A, Węglarczyk K, Rutkowska M, Baj-Krzyworzeka M, Pituch-Noworolska A, Kowalczyk D, Grodzicki T, Ziegler-Heitbrock L, Zembala M
    We have studied the effect of intravenous immunoglobulins (IVIG) on monocyte subpopulations and cytokine production in patients with CVID. The absolute number of CD14(+)CD16(++) monocytes decreased on average 2.5-fold 4h after IVIG and after 20h returned to the baseline. The cytokine level in the supernatants of peripheral blood mononuclear cells (PBMC) after ex vivo LPS stimulation demonstrated the &amp;gt;2-fold decrease in TNF production 4h after IVIG. The TNF expression, which is higher in the CD14(+)CD16(++) monocytes, was decreased in these cells by IVIG in 4/7 CVID cases. In vitro expos...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4479680</comments>
            <pubDate>Sat, 15 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4479680</guid>        </item>
        <item>
            <title>Paucity of genotype-phenotype correlations in STAT3 mutation positive Hyper IgE Syndrome (HIES).</title>
            <link>http://www.medworm.com/index.php?rid=4479686&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21288777%26dopt%3DAbstract</link>
            <description>Authors: Heimall J, Davis J, Shaw PA, Hsu AP, Gu W, Welch P, Holland SM, Freeman AF
    Autosomal dominant HIES (AD-HIES) is a primary immunodeficiency caused by dominant negative mutations in STAT3 clustered in the DNA binding and SH2 domains. Although in vitro differences in mutational constructs are observed, clinical phenotypic correlates of these genetic changes have not been described. We reviewed the charts of 65 AD-HIES patients (DNA binding n=35; SH2 n=30), recorded the components of the NIH HIES clinical scoring system as well as brain and coronary artery abnormalities and analyzed data by mutation region in adults and children. Patients with SH2 domain mutations had increased frequency of high palate, broad inter-alar distance, upper respiratory tract infections and, in the pedi...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4479686</comments>
            <pubDate>Fri, 14 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4479686</guid>        </item>
        <item>
            <title>Diagnostic criteria of inflammatory bowel disease.</title>
            <link>http://www.medworm.com/index.php?rid=4350044&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21233020%26dopt%3DAbstract</link>
            <description>Authors: Xue L, Ouyang Q
    
    PMID: 21233020 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4350044</comments>
            <pubDate>Tue, 11 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4350044</guid>        </item>
        <item>
            <title>Allergen-stimulated production of intracellular ROS in neutrophils: Yes but questions remain.</title>
            <link>http://www.medworm.com/index.php?rid=4350043&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21233021%26dopt%3DAbstract</link>
            <description>Authors: Mora J, Riggs EK, Fu J, Macglashan DW, Fox SA, Yu B, Tobin MC, Thomas LL
    
    PMID: 21233021 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4350043</comments>
            <pubDate>Tue, 11 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4350043</guid>        </item>
        <item>
            <title>Harnessing natural killer T (NKT) cells in human myeloma: Progress and challenges.</title>
            <link>http://www.medworm.com/index.php?rid=4350042&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21233022%26dopt%3DAbstract</link>
            <description>Authors: Dhodapkar MV, Richter J
    Multiple myeloma is a hematologic malignancy characterized by growth of malignant plasma cells in the bone marrow. Tumor cells in myeloma express CD1d and are sensitive to lysis by CD1d restricted natural killer T (NKT) cells. Here we discuss recent studies to harness the properties of these cells in the context of human myeloma. In spite of large body of preclinical data, attempts to fully harness the properties of these cells in the clinic are in early stages. Early phase clinical studies document the capacity of human monocyte-derived dendritic cells to expand NKT cells in vivo in myeloma patients. These results have set the stage for ongoing studies combining NKT activation with immune-modulatory drugs. Lessons learnt from these studies may inform t...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4350042</comments>
            <pubDate>Tue, 11 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4350042</guid>        </item>
        <item>
            <title>IFN-α cannot substitute lack of IFN-γ responsiveness in cells of an IFN-γR1 deficient patient.</title>
            <link>http://www.medworm.com/index.php?rid=4350045&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21216674%26dopt%3DAbstract</link>
            <description>In conclusion, no evidence was found to support the use of IFN-α in IFN-γR-deficient patients as intervention against mycobacterial infection; on the contrary, treatment of individuals with IFN-α may even adversely affect host defence against Mycobacteria.
    PMID: 21216674 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4350045</comments>
            <pubDate>Fri, 07 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4350045</guid>        </item>
        <item>
            <title>OPN promotes survival of activated T cells by up-regulating CD44 in oral lichen planus patient.</title>
            <link>http://www.medworm.com/index.php?rid=4350047&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21215700%26dopt%3DAbstract</link>
            <description>Authors: Liu GX, Sun JT, Yang MX, Qi XM, Shao QQ, Xie Q, Qu X, Wei FC, Sun SZ
    Oral lichen planus (OLP) is a chronic inflammatory disorder of oral mucosa, which represents cell-mediated autoimmune diseases. Pathological study demonstrated that abundant T lymphocytes infiltrated the oral mucosa, in which the activated T cells that trigger apoptosis of oral epithelial cells is an important mechanism for OLP. However, to date the molecular mechanisms underlying the T lymphocytes infiltration and accumulation in OLP remain unclear. In this paper, we found that the levels of plasma OPN were elevated and were associated with the up-regulated expressions of CD44 in OLP patients. In vitro, the addition of exogenous OPN can suppress the apoptosis of activated CD8(+) T cells via CD44, and this T ...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4350047</comments>
            <pubDate>Wed, 05 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4350047</guid>        </item>
        <item>
            <title>Are the reference values of B cell subpopulations used in adults for classification of common variable immunodeficiencies appropriate for children?</title>
            <link>http://www.medworm.com/index.php?rid=4350046&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21215701%26dopt%3DAbstract</link>
            <description>Authors: Smet J, Mascart F, Schandené L
    Detailed phenotypic characterization of B cell subpopulations is of utmost importance for the diagnosis and management of humoral immunodeficiencies, as they are used for classification of common variable immunodeficiencies. Since age-specific reference values remain scarce in the literature, we analysed by flow cytometry the proportions and absolute values of total, memory, switched memory and CD21(-/low) B cells in blood samples from 168 healthy children (1day to 18years) with special attention to the different subpopulations of CD21(low) B cells. The percentages of total memory B cells and their subsets significantly increased up to 5-10years. In contrast, the percentages of immature CD21(-) B cells and of immature transitional CD21(low)CD38(...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4350046</comments>
            <pubDate>Wed, 05 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4350046</guid>        </item>
        <item>
            <title>Strategy for anti-aquaporin-4 auto-antibody identification and quantification using a new cell-based assay.</title>
            <link>http://www.medworm.com/index.php?rid=4350048&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21190899%26dopt%3DAbstract</link>
            <description>In conclusion, we propose to use IIF for the screening of patients at diagnosis in order to identify auto-Abs targeting the central nervous system. A highly sensitive, AQP4 specific and quantitative assay such as our CBA could be used thereafter to specifically identify the target of the Ab and to monitor its serum concentration under treatment.
    PMID: 21190899 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4350048</comments>
            <pubDate>Mon, 27 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4350048</guid>        </item>
        <item>
            <title>Clinical development of a novel CD1d-binding NKT cell ligand as a vaccine adjuvant.</title>
            <link>http://www.medworm.com/index.php?rid=4350052&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21185784%26dopt%3DAbstract</link>
            <description>Authors: Padte NN, Li X, Tsuji M, Vasan S
    Natural killer T (NKT) cells are known to play a role against certain microbial infections, including malaria and HIV, two major global infectious diseases. Strategies that can harness and amplify the immunotherapeutic potential of NKT cells can serve as powerful tools in the fight against such diseases. 7DW8-5, a novel glycolipid, may be one such tool. The interaction of 7DW8-5 with CD1d molecules induces activation of NKT cells, thereby activating various immune-competent cells including dendritic cells (DCs) to provide a significant adjuvant effect for several vaccines. This review discusses the discovery and characterization of 7DW8-5 and the practical considerations of its preclinical and clinical development as a potential glycolipid adju...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4350052</comments>
            <pubDate>Thu, 23 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4350052</guid>        </item>
        <item>
            <title>On the use of donor-derived iNKT cells for adoptive immunotherapy to prevent leukemia recurrence in pediatric recipients of HLA haploidentical HSCT for hematological malignancies.</title>
            <link>http://www.medworm.com/index.php?rid=4350051&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21185785%26dopt%3DAbstract</link>
            <description>Authors: Dellabona P, Casorati G, de Lalla C, Montagna D, Locatelli F
    T-cell-depleted hematopoietic stem cell transplantation from an HLA haploidentical relative (hHSCT) is a useful therapy for children with high-risk leukemia lacking suitable HLA-matched donors. The immune deficiency ensuing hHSCT renders patients susceptible to life-threatening infections and disease recurrence. Adoptive immunotherapy can restore/enhance early post-transplantation immunocompetence of hHSCT recipients. Efforts are directed to identify strategies for inducing graft-versus-leukemia (GVL) response, while avoiding graft-versus-host disease (GVHD) occurrence. CD1d-restricted invariant iNKT cells are innate-like, lipid-reactive T lymphocytes implicated in the control of innate and adaptive immunity. Preclin...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4350051</comments>
            <pubDate>Thu, 23 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4350051</guid>        </item>
        <item>
            <title>High level of soluble HLA-G in amniotic fluid is correlated with congenital transmission of Toxoplasma gondii.</title>
            <link>http://www.medworm.com/index.php?rid=4350050&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21185786%26dopt%3DAbstract</link>
            <description>Authors: Robert-Gangneux F, Gangneux JP, Vu N, Jaillard S, Guiguen C, Amiot L
    The expression of human leukocyte antigen (HLA)-G on cytotrophoblast cells contributes to maternal-fetal tolerance. Soluble forms of HLA-G (sHLA-G) can be detected in amniotic fluid (AF) and a decrease of sHLA-G is known to be correlated to fetal loss. In this work we investigated the role of sHLA-G in the transplacental passage of the protozoan parasite Toxoplasma gondii, responsible for congenital toxoplasmosis in about 30% of fetuses when primary infection (PI) occurs during pregnancy. We determined the sHLA-G concentration in 61 AF from women with PI and 24 controls. Our results showed higher sHLA-G levels in AF from PI than in controls (p&amp;lt;0.001). Moreover sHLA-G level from congenitally infected fetuse...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4350050</comments>
            <pubDate>Thu, 23 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4350050</guid>        </item>
        <item>
            <title>Induction of NKT cell-specific immune responses in cancer tissues after NKT cell-targeted adoptive immunotherapy.</title>
            <link>http://www.medworm.com/index.php?rid=4350049&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21185787%26dopt%3DAbstract</link>
            <description>Authors: Yamasaki K, Horiguchi S, Kurosaki M, Kunii N, Nagato K, Hanaoka H, Shimizu N, Ueno N, Yamamoto S, Taniguchi M, Motohashi S, Nakayama T, Okamoto Y
    Vα24 natural killer T (NKT) cells have potent anti-tumor activity. We performed a phase II clinical study in patients with head and neck squamous cell carcinoma (HNSCC) using ex vivo expanded Vα24 NKT cells and α-galactosylceramide (αGalCer; KRN7000)-pulsed antigen-presenting cells (APCs) to investigate the efficacy and induction of NKT cell-specific immune responses. The subjects were 10 patients with locally recurrent and operable HNSCC. One course of nasal submucosal administration of αGalCer-pulsed APCs and intra-arterial infusion of activated NKT cells via tumor-feeding arteries was given before salvage surgery. Anti-tumor ...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4350049</comments>
            <pubDate>Thu, 23 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4350049</guid>        </item>
        <item>
            <title>Clinical experience with α-galactosylceramide (KRN7000) in patients with advanced cancer and chronic hepatitis B/C infection.</title>
            <link>http://www.medworm.com/index.php?rid=4350054&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21169066%26dopt%3DAbstract</link>
            <description>Authors: Schneiders FL, Scheper RJ, von Blomberg BM, Woltman AM, Janssen HL, van den Eertwegh AJ, Verheul HM, de Gruijl TD, van der Vliet HJ
    For over a century, research has sought ways to boost the immune system in order to eradicate tumors and viruses that exist after escaping immunosurveillance. For the treatment of cancer and hepatitis immunotherapeutic strategies have overall had limited clinical success. An urgent need exists therefore to introduce more effective therapeutic approaches. Invariant (i)NKT cells constitute a conserved T lymphocyte lineage with dominant immunoregulatory, antitumor and antiviral effector cell properties. iNKT specifically recognize the glycolipid α-galactosylceramide in the context of CD1d resulting in their activation. Activated iNKT can promote the...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4350054</comments>
            <pubDate>Fri, 17 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4350054</guid>        </item>
        <item>
            <title>Temporal dynamics of anti-MOG antibodies in CNS demyelinating diseases.</title>
            <link>http://www.medworm.com/index.php?rid=4350053&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21169067%26dopt%3DAbstract</link>
            <description>Authors: Di Pauli F, Mader S, Rostasy K, Schanda K, Bajer-Kornek B, Ehling R, Deisenhammer F, Reindl M, Berger T
    Recent studies demonstrated the presence of autoantibodies to native myelin oligodendrocyte glycoprotein (MOG) in juvenile patients with acute disseminated encephalomyelitis (ADEM) and multiple sclerosis (MS). However, so far no longitudinal studies on anti-MOG antibodies have been performed. Therefore, we determined serum and CSF antibodies against native human MOG in 266 pediatric and adult subjects with ADEM, clinically isolated syndrome (CIS), MS, other neurological diseases (OND) and healthy controls (HC) and longitudinal samples of 25 patients with ADEM, CIS, MS and OND using an immunofluorescence assay. We detected serum high-titer MOG IgG in 15/34 (44%) patients with...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4350053</comments>
            <pubDate>Fri, 17 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4350053</guid>        </item>
        <item>
            <title>1α,25-dihydroxyvitamin D3 (vitamin D3) catalyzes suppressive activity on human natural regulatory T cells, uniquely modulates cell cycle progression, and augments FOXP3.</title>
            <link>http://www.medworm.com/index.php?rid=4350055&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21167785%26dopt%3DAbstract</link>
            <description>Authors: Morales-Tirado V, Wichlan DG, Leimig TE, Street SE, Kasow KA, Riberdy JM
    Human natural regulatory T cells (nTregs) show great promise for therapeutically modulating immune-mediated disease, but remain poorly understood. One explanation under intense scrutiny is how to induce suppressive function in non-nTregs and increase the size of the regulatory population. A second possibility would be to make existing nTregs more effective, like a catalyst raises the specific activity of an enzyme. The latter has been difficult to investigate due to the lack of a robust short-term suppression assay. Using a microassay described herein we demonstrate that nTregs in distinct phases of cell cycle progression exhibit graded degrees of potency. Moreover, we show that physiological concentratio...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4350055</comments>
            <pubDate>Wed, 15 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4350055</guid>        </item>
        <item>
            <title>Florfenicol inhibits allergic airway inflammation in mice by p38 MAPK-mediated phosphorylation of GATA 3.</title>
            <link>http://www.medworm.com/index.php?rid=4350057&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21163707%26dopt%3DAbstract</link>
            <description>Authors: Xinxin C, Chi C, Xiao C, Xue X, Yongjun Y, Junqing C, Xuming D
    Florfenicol has been shown to possess anti-inflammatory activity. However, its possible use for asthma has not yet been studied. First we investigated the anti-inflammatory properties of florfenicol using mice asthma model. BALB/c mice were immunized and challenged by ovalbumin. Treatment with florfenicol caused a marked reduction in inflammatory cells and three Th2 type cytokines in the bronchoalveolar lavage fluids of mice. The levels of ovalbumin-specific IgE and airway hyperresponsiveness were significantly altered after treatment with florfenicol. Histological studies using H&amp;E and AB-PAS staining demonstrate that florfenicol substantially inhibited ovalbumin-induced inflammatory cells infiltration in lung...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4350057</comments>
            <pubDate>Tue, 14 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4350057</guid>        </item>
        <item>
            <title>DNA-based vaccines for multiple sclerosis: Current status and future directions.</title>
            <link>http://www.medworm.com/index.php?rid=4350056&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21163708%26dopt%3DAbstract</link>
            <description>Authors: Fissolo N, Montalban X, Comabella M
    Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system that mainly affects young adults between 20 and 40years of age and leads to significant disability. Although MS is considered to be an immune-mediated disorder, current immunosuppressive therapies fail to inhibit disease progression, and some of them are associated with serious adverse reactions. DNA vaccination is a strategy of immunization based on the injection of genes encoding for target proteins. Depending on the route as well as the dosage of administration, exposure to certain molecules may either stimulate effector responses or induce immune tolerance. A large body of data from the animal model, experimental autoimmune encephalomyelitis (EAE), ha...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4350056</comments>
            <pubDate>Tue, 14 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4350056</guid>        </item>
        <item>
            <title>Oral priming with Salmonella Typhi vaccine strain CVD 909 followed by parenteral boost with the S. Typhi Vi capsular polysaccharide vaccine induces CD27(+)IgD(-)S. Typhi-specific IgA and IgG B memory cells in humans.</title>
            <link>http://www.medworm.com/index.php?rid=4350058&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21146460%26dopt%3DAbstract</link>
            <description>Authors: Wahid R, Pasetti MF, Maciel M, Simon JK, Tacket CO, Levine MM, Sztein MB
    Attenuated live oral typhoid vaccine candidate CVD 909 constitutively expresses Salmonella Typhi capsular polysaccharide antigen (Vi). A randomized, double-blind, heterologous prime-boost clinical study was conducted to determine whether immunity to licensed parenteral Vi vaccine could be enhanced by priming with CVD 909. Priming with CVD 909 elicited higher and persistent, albeit not significant, anti-Vi IgG and IgA following immunization with Vi, than placebo-primed recipients. Vi-specific IgA B memory (B(M)) cells were significantly increased in CVD 909-primed subjects. S. Typhi-specific LPS and flagella IgA B(M) cells were observed in subjects immunized with CVD 909 or with the licensed Vi-negative or...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4350058</comments>
            <pubDate>Thu, 09 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4350058</guid>        </item>
        <item>
            <title>Murine autoimmune hearing loss mediated by CD4(+) T cells specific for β-tubulin.</title>
            <link>http://www.medworm.com/index.php?rid=4350059&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21145286%26dopt%3DAbstract</link>
            <description>Authors: Zhou B, Kermany MH, Glickstein J, Cai Q, Cai C, Zhou Y, Nair U, Kim JW, Kim P, Liu W, Kanangat S, Yoo TJ
    Autoimmune inner ear disease is described as progressive, bilateral although asymmetric, sensorineural hearing loss and can be improved by immunosuppressive therapy. We showed that the inner ear autoantigen β-tubulin is capable of inducing experimental autoimmune hearing loss (EAHL) in mice. Immunization of BALB/c mice with β-tubulin resulted in hair cell loss and hearing loss, effects that were not seen in animals immunized with control peptide. Moreover, the EAHL model showed that β-tubulin responsiveness involved CD4(+) T cells producing IFN-γ, and T cell mediation of EAHL was determined by significantly increased auditory brainstem response after adoptive transfer o...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4350059</comments>
            <pubDate>Wed, 08 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4350059</guid>        </item>
        <item>
            <title>Analysis of mutations and recombination activity in RAG-deficient patients.</title>
            <link>http://www.medworm.com/index.php?rid=4253672&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21131235%26dopt%3DAbstract</link>
            <description>Authors: Asai E, Wada T, Sakakibara Y, Toga A, Toma T, Shimizu T, Nampoothiri S, Imai K, Nonoyama S, Morio T, Muramatsu H, Kamachi Y, Ohara O, Yachie A
    Mutations in the recombination activating genes (RAG1 or RAG2) can lead to a variety of immunodeficiencies. Herein, we report 5 cases of RAG deficiency from 5 families: 3 of Omenn syndrome, 1 of severe combined immunodeficiency, and 1 of combined immunodeficiency with oligoclonal TCRγδ(+) T cells, autoimmunity and cytomegalovirus infection. The genetic defects were heterogeneous and included 6 novel RAG mutations. All missense mutations except for Met443Ile in RAG2 were located in active core regions of RAG1 or RAG2. V(D)J recombination activity of each mutant was variable, ranging from half of the wild type activity to none, however,...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4253672</comments>
            <pubDate>Fri, 03 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4253672</guid>        </item>
        <item>
            <title>The basal activation state of DC subsets correlates with anti-HCV treatment outcome in HCV/HIV co-infected patients.</title>
            <link>http://www.medworm.com/index.php?rid=4253674&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21130688%26dopt%3DAbstract</link>
            <description>Authors: Sacchi A, Agrati C, D'Offizi G, Vlassi C, Rozera G, Abbate I, Capobianchi MR, Martini F
    In this work we evaluated plasmacytoid (pDC) and myeloid dendritic (mDC) cells activation before and during anti-HCV treatment in HCV+/HIV+ individuals. HCV+/HIV+ patients received Peg-IFN-α2b subcutaneously for 28days, followed by oral weight-based ribavirin. DCs activation was evaluated by flow cytometry. Baseline pDC CD80 and CD86 expression was correlated with HIV, but not with HCV viral load. A transient decrease of HIV RNA was found not associated with DC activation. When patients were grouped according to early/sustained virological response (EVR/SVR) to anti-HCV treatment, baseline pDC CD80 and CD86 expression was higher in non-EVR and non-SVR compared to EVR and SVR. Moreover, in ...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4253674</comments>
            <pubDate>Thu, 02 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4253674</guid>        </item>
        <item>
            <title>Preferential enhancement of older human T cell cytokine generation, chemotaxis, proliferation and survival by lenalidomide.</title>
            <link>http://www.medworm.com/index.php?rid=4253677&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21130040%26dopt%3DAbstract</link>
            <description>Authors: Huang MC, Greig NH, Luo W, Tweedie D, Schwartz JB, Longo DL, Ferrucci L, Ershler WB, Goetzl EJ
    Lenalidomide, an analog of thalidomide, modified responses of stimulated T cells from healthy young (ages 21-40years) and old (≥age 65years) subjects. At 0.03μM to 1μM, lenalidomide enhanced generation of IL-2 and IFN-γ by T cell receptor-stimulated T cells of young subjects up to respective maximum increases of 17-fold and three-fold, but at 0.3μM and 1μM suppressed IL-17 generation. The same concentrations of lenalidomide enhanced IL-2 and IFN-γ generation by stimulated T cells of old subjects more, with greater respective maximal increases of up to 120-fold and six-fold, without suppressing IL-17 generation. Lenalidomide enhanced proliferation and suppressed apoptosis of s...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4253677</comments>
            <pubDate>Wed, 01 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4253677</guid>        </item>
        <item>
            <title>Intravenous immunoglobulins exposed to heme (heme IVIG) are more efficient than IVIG in attenuating autoimmune diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=4253680&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21123117%26dopt%3DAbstract</link>
            <description>We examined the effect of IVIG and heme-exposed IVIG on the development of immune mediated diabetes induced in C57BL/6 mice by multiple low doses of streptozotocin. IVIG were used in a dose of 200mg/kg daily for 15days. Treatment with IVIG resulted in significant attenuation of diabetes induction as evaluated by glycemia, glycosuria and HbA1c level. Interestingly, heme-exposed IVIG had a still stronger antidiabetogenic effect. Serum levels of proinflammatory cytokines TNF-α, IFN-γ and IL17 were lower in IVIG treated animals when compared with controls, while IL10 level was higher. The number of CD4(+)Foxp3(+) cells was higher in pancreatic lymph nodes of heme-exposed IVIG treated mice. Our results show that IVIG may downregulate diabetes induction possibly by favouring induction of T reg...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4253680</comments>
            <pubDate>Mon, 29 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4253680</guid>        </item>
        <item>
            <title>Anti-tumor potential of type-I NKT cells against CD1d-positive and CD1d-negative tumors in humans.</title>
            <link>http://www.medworm.com/index.php?rid=4203488&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21095162%26dopt%3DAbstract</link>
            <description>Authors: Metelitsa LS
    Vα24-invariant natural killer T cells (NKTs) are strictly CD1d-restricted, and CD1d expression has been found in several types of leukemia and lymphoma as well as in brain tumors suggesting that these malignancies could be targeted for direct NKT-cell cytotoxicity. Several studies have revealed strong positive associations between the numbers of tumor-infiltrating or circulating NKTs with improved disease outcome in patients with diverse types of CD1d-negative solid tumors. The mechanism by which NKTs mediate anti-tumor activity against CD1d-negative tumors has long remained enigmatic. Recent evidence indicates that NKTs can suppress tumor growth indirectly by targeting CD1d-positive elements of tumor-supportive stroma such as tumor-associated macrophages. This r...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4203488</comments>
            <pubDate>Sat, 20 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4203488</guid>        </item>
        <item>
            <title>Phosphatidylserine reduces immune response against human recombinant Factor VIII in Hemophilia A mice by regulation of dendritic cell function.</title>
            <link>http://www.medworm.com/index.php?rid=4203489&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21094627%26dopt%3DAbstract</link>
            <description>Authors: Gaitonde P, Peng A, Straubinger RM, Bankert RB, Balu-Iyer SV
    A major clinical complication in the treatment of Hemophilia A using exogenously administered recombinant Factor VIII (FVIII) is the development of neutralizing antibodies. It has been shown previously that FVIII complexed with phosphatidylserine (PS) reduces the development of total and neutralizing antibody titers in hemophilic mice. The effect of complexation of FVIII with PS upon dendritic cell (DC) uptake, maturation and processing, T-cell proliferation and cytokine secretion profiles was investigated. Flow cytometric studies of DC showed that PS inhibited the up-regulation of cell surface co-stimulatory markers (CD86 and CD40). PS reduced T-cell proliferation and significantly increased levels of TGF-β and IL-...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4203489</comments>
            <pubDate>Fri, 19 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4203489</guid>        </item>
        <item>
            <title>Circulating cytokines are associated with human islet graft function in type 1 diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=4203490&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21094094%26dopt%3DAbstract</link>
            <description>Authors: Pfleger C, Schloot NC, Brendel MD, Burkart V, Hogenkamp V, Bretzel RG, Jaeger C, Eckhard M
    Islet cell transplantation has considerable potential as a cure for type 1 diabetes, but recurrent autoimmunity and allograft rejection in which both cytokines play an important role are major obstacles. Using a new approach considering confounders by regression analysis, we investigated circulating cytokines and their association with graft function in type 1 diabetes patients who underwent either simultaneous islet kidney (SIK) or islet after kidney (IAK) transplantation. After transplantation, interleukin (IL)-10 was lower in SIK recipients with subsequent loss of graft function in comparison to recipients maintaining graft function. Before transplantation, high IL-13 and IL-18 concen...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4203490</comments>
            <pubDate>Thu, 18 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4203490</guid>        </item>
        <item>
            <title>Development of gut-homing receptors on circulating B cells during infancy.</title>
            <link>http://www.medworm.com/index.php?rid=4170519&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21075690%26dopt%3DAbstract</link>
            <description>In conclusion, the high fraction of circulating IgA+ and IgG+ B cells expressing CCR9 and CCR10 in the first months of life indicates activation of naïve B cells in the gut, coinciding with bacterial colonization.
    PMID: 21075690 [PubMed - as supplied by publisher] (Source: Clinical Immunology)</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4170519</comments>
            <pubDate>Fri, 12 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4170519</guid>        </item>
        <item>
            <title>Identification of a novel linear epitope on EspA from enterohemorrhagic E. coli using a neutralizing and protective monoclonal antibody.</title>
            <link>http://www.medworm.com/index.php?rid=4170518&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21075691%26dopt%3DAbstract</link>
            <description>Authors: Yu S, Gu J, Wang HG, Wang QX, Luo P, Wu C, Zhang WJ, Guo G, Tong WD, Zou QM, Mao XH
    Enterohemorrhagic E. coli (EHEC) causes severe diseases in humans and animals via the production of Shiga toxins, and injection of effectors into epithelia using type III secretion system (TTSS). E. coli secreted protein A (EspA) forms the filamentous conduits of TTSS, which extends into the translocation pore embedded in host cell membranes and aids in the transportation of bacterial effectors. In addition, EspA is closely associated with initial bacterial adhesion and the formation of biofilms. EspA in its various forms elicits protective immune responses, although the epitope responsible has not to be identified. Here we report the presence of a linear, immunogenic, conserved and partially p...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4170518</comments>
            <pubDate>Fri, 12 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4170518</guid>        </item>
        <item>
            <title>Reversion of resistance to immunosuppressive agents in three patients with psoriatic arthritis by cyclosporine A: Modulation of P-glycoprotein function.</title>
            <link>http://www.medworm.com/index.php?rid=4170521&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21062675%26dopt%3DAbstract</link>
            <description>Authors: Diamanti AP, Rosado M, Germano V, Scarsella M, Giorda E, Podestà E, D'Amelio R, Carsetti R, Laganà B
    Secondary resistance may be a major problem in the management of autoimmune diseases. P-glycoprotein (P-gp) over-function has been described as a mechanism of drug resistance in autoimmune patients. P-gp function can in vitro be inhibited by cyclosporine A (CSA) and verapamil; moreover, P-gp reduction by CSA in systemic lupus erythematosus and rheumatoid arthritis has been demonstrated. Here, P-gp function before and after CSA administration in three psoriatic arthritis (PsA) patients, who developed a resistance to MTX/SSA, has been evaluated. P-gp function on patient cells was analyzed by measuring the changes in rhodamine-123 (Rh-123) fluorescence after verapamil incubation...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4170521</comments>
            <pubDate>Mon, 08 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4170521</guid>        </item>
        <item>
            <title>Differences in the humoral autoreactivity to zinc transporter 8 between childhood- and adult-onset type 1 diabetes in Japanese patients.</title>
            <link>http://www.medworm.com/index.php?rid=4170520&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21067978%26dopt%3DAbstract</link>
            <description>Authors: Kawasaki E, Nakamura K, Kuriya G, Satoh T, Kobayashi M, Kuwahara H, Abiru N, Yamasaki H, Matsuura N, Miura J, Uchigata Y, Eguchi K
    The aim of this study was to evaluate the humoral autoreactivity to zinc transporter 8 (ZnT8) depending on the clinical phenotype of type 1 diabetes (T1D). ZnT8 autoantibodies (ZnT8A) were determined by radioimmunoassay using carboxy-terminal ZnT8 constructs in 57 childhood-onset, 97 adult-onset, and 85 fulminant T1D. The ZnT8A frequency was higher in childhood-onset patients and decreased with increasing age of onset from 70% to 24% (P(trend)&amp;lt;0.005). None of the patients with fulminant T1D was positive for ZnT8A. There were at least two distinct ZnT8A epitope patterns associated with the aa325-restriction, childhood-onset patients have aa325-no...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4170520</comments>
            <pubDate>Mon, 08 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4170520</guid>        </item>
        <item>
            <title>Tremelimumab (anti-CTLA4) mediates immune responses mainly by direct activation of T effector cells rather than by affecting T regulatory cells.</title>
            <link>http://www.medworm.com/index.php?rid=4170523&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21056008%26dopt%3DAbstract</link>
            <description>Authors: Khan S, Burt DJ, Ralph C, Thistlethwaite FC, Hawkins RE, Elkord E
    Cytotoxic T Lymphocyte Antigen 4 (CTLA4) blockade has shown antitumor activity against common cancers. However, the exact mechanism of immune mediation by anti-CTLA4 remains to be elucidated. Further understanding of how CTLA4 blockade with tremelimumab mediates immune responses may allow a more effective selection of responsive patients. Our results show that tremelimumab enhanced the proliferative response of T effector cells (Teff) upon TCR stimulation, and abrogated Treg suppressive ability. In the presence of tremelimumab, frequencies of IL-2-secreting CD4(+) T cells and IFN-γ-secreting CD4(+) and CD8(+) T cells were increased in response to polyclonal activation and tumor antigens. Importantly, Treg frequ...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4170523</comments>
            <pubDate>Wed, 03 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4170523</guid>        </item>
        <item>
            <title>Synovial fluid-derived T helper 17 cells correlate with inflammatory activity in arthritis, irrespectively of diagnosis.</title>
            <link>http://www.medworm.com/index.php?rid=4170522&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21056009%26dopt%3DAbstract</link>
            <description>Authors: Zizzo G, De Santis M, Bosello SL, Fedele AL, Peluso G, Gremese E, Tolusso B, Ferraccioli G
    We analyzed peripheral blood (PB) and synovial fluid (SF) mononuclear cells from 16 rheumatoid arthritis (RA), 9 spondyloarthritis (SpA), 3 microcrystal arthritis patients, to define the presence of Th17 and Th1 and their relationship with inflammatory activity, and TCR-zeta chain and ZAP-70 levels. Th17 were significantly higher in SF than in PB and more abundant in microcrystal arthritis patients compared to the other groups. Irrespectively of the diagnosis, SF Th17 percentages correlated with joint (SF total leukocyte count, neutrophil percentage) and systemic (C reactive protein [CRP], fibrinogen, erythrocyte sedimentation rate) inflammation markers. SF Th1 percentages directly corre...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4170522</comments>
            <pubDate>Wed, 03 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4170522</guid>        </item>
        <item>
            <title>GAD-alum treatment induces GAD(65)-specific CD4(+)CD25(high)FOXP3(+) cells in type 1 diabetic patients.</title>
            <link>http://www.medworm.com/index.php?rid=4140212&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21044870%26dopt%3DAbstract</link>
            <description>Authors: Hjorth M, Axelsson S, Rydén A, Faresjö M, Ludvigsson J, Casas R
    Type 1 diabetes results from autoimmune destruction of insulin producing pancreatic β-cells. We have shown that treatment with alum-formulated glutamic acid decarboxylase 65 (GAD-alum) preserved residual insulin secretion and induced antigen-specific responses in children with recent onset type 1 diabetes. The aim of this study was to further investigate the immunomodulatory effect of GAD-alum, focusing on CD4(+)CD25(high) cells and their association to cytokine secretion. Samples obtained 21 and 30months after the initial injection of GAD-alum or placebo were included in the present study. GAD(65)-stimulation enhanced the percentage of CD4(+)CD25(high)FOXP3(+) cells, but reduced the percentage of CD4(+)CD25(+)...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4140212</comments>
            <pubDate>Sun, 31 Oct 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4140212</guid>        </item>
        <item>
            <title>Immune modulation and safety profile of adoptive immunotherapy using expanded autologous activated lymphocytes against advanced cancer.</title>
            <link>http://www.medworm.com/index.php?rid=4140213&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21041120%26dopt%3DAbstract</link>
            <description>In this study, 19 patients with metastatic tumors received EAAL therapy. Two to four weeks after the administration of EAAL cells, the subsets of CD3(+)CD8(+) T lymphocytes and CD3(-)CD56(+) natural killer cells in the peripheral blood were increased significantly in comparison with those before the therapy. The number of IFN-γ secreting cells also significantly increased after the EAAL infusion (p=0.002) and the p values for the counts of CD3(+)IFN-γ(+) lymphocytes and CD3(-)IFN-γ(+) lymphocytes were 0.006 and 0.015, respectively. Moreover, the percentage of IFN-γ producing cells of the CD3(+), CD8(+) and CD3(-) subsets after infusion were all increased significantly, which indicated that EAAL therapy was able to enrich the potentially anti-tumor cytotoxic peripheral blood lymphocytes...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4140213</comments>
            <pubDate>Sat, 30 Oct 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4140213</guid>        </item>
        <item>
            <title>Early vs. delayed diagnosis of severe combined immunodeficiency: A family perspective survey.</title>
            <link>http://www.medworm.com/index.php?rid=4140214&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21035402%26dopt%3DAbstract</link>
            <description>Authors: Chan A, Scalchunes C, Boyle M, Puck JM
    Infants affected with severe combined immunodeficiency (SCID) are susceptible to severe and recurrent infections and do not survive unless provided with immune reconstituting treatments. In the absence of population-based newborn screening, infants with SCID who do not have an affected older relative are ascertained only after they have developed infections. However, only limited data are available from the perspective of patients and families to indicate what proportion of SCID cases might benefit from earlier detection by pre-symptomatic screening, whether adequate treatment facilities are available, and how screening could improve SCID treatment outcomes. A survey of parents of children with SCID evaluated family history, pre- and post...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4140214</comments>
            <pubDate>Wed, 27 Oct 2010 00:00:00 +0100</pubDate>
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            <title>High levels of Crohn's disease-associated anti-microbial antibodies are present and independent of colitis in chronic granulomatous disease.</title>
            <link>http://www.medworm.com/index.php?rid=4091762&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20956091%26dopt%3DAbstract</link>
            <description>Authors: Yu JE, De Ravin SS, Uzel G, Landers C, Targan S, Malech HL, Holland SM, Cao W, Harpaz N, Mayer L, Cunningham-Rundles C
    Chronic granulomatous disease (CGD) and inflammatory bowel disease (IBD) have overlapping gastrointestinal manifestations. Serum antibodies to intestinal microbial antigens in IBD are thought to reflect a loss of tolerance in the setting of genetically encoded innate immune defects. CGD subjects studied here, with or without colitis, had considerably higher levels of ASCA IgA, ASCA IgG, anti-OmpC, anti-I2, and anti-CBir1, but absent to low pANCA, compared to IBD-predictive cutoffs. Higher antibody levels were not associated with a history of colitis. Except for higher ASCA IgG in subjects &amp;lt;18years, antibody levels were not age-dependent. In comparison, 7 HI...</description>
            <author>Clinical Immunology</author>
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            <pubDate>Fri, 15 Oct 2010 23:00:00 +0100</pubDate>
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            <title>Specific cytokine patterns of pulmonary tuberculosis in Central Africa.</title>
            <link>http://www.medworm.com/index.php?rid=4091763&amp;cid=s_33853_3_f&amp;fid=33853&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20951096%26dopt%3DAbstract</link>
            <description>Authors: Nemeth J, Winkler HM, Boeck L, Adegnika AA, Clement E, Mve TM, Kremsner PG, Winkler S
    Different cytokines have been suggested to be involved in the pathogenesis of pulmonary tuberculosis (TB). The frequencies of Mycobacterium tuberculosis (MTB) specific CD4(+) and CD8(+) T cells, CD4(+)CD25(+) Forkhead Box Protein (FoxP)3(+) T cells, interleukin (IL)-6, interferon (IFN)-γ, Tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β and IL-10 were assessed in HIV-negative, pulmonary tuberculosis (TB) patients (n=30) and in healthy controls (n=23) in Gabon. Peripheral blood mononuclear cells (PBMC) were stimulated with purified protein derivative (PPD) and early secretory antigenic target-6 (ESAT-6). In patients, a pronounced pro-inflammatory cytokine response with high...</description>
            <author>Clinical Immunology</author>
            <type>journals</type>
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            <pubDate>Tue, 12 Oct 2010 23:00:00 +0100</pubDate>
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