<?xml version="1.0" encoding="UTF-8"?>
<rss version="2.0">
    <channel>
        <title>Journal of Leukocyte Biology 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 'Journal of Leukocyte Biology' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Journal+of+Leukocyte+Biology&t=Journal+of+Leukocyte+Biology&s=Search&f=source]]></link>
        <lastBuildDate>Wed, 08 Feb 2012 17:42:05 +0100</lastBuildDate>
        <item>
            <title>Reprogramming of TAM toward proimmunogenic type through regulation of MAP kinases using a redox-active copper chelate.</title>
            <link>http://www.medworm.com/index.php?rid=5644043&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22279179%26dopt%3DAbstract</link>
            <description>Authors: Chakraborty P, Chatterjee S, Ganguly A, Saha P, Adhikary A, Das T, Chatterjee M, Choudhuri SK
    Abstract
    TAMs, present in the tumor microenvironment, play an immunosuppressive role, leading to tumor progression and metastasis. Recently, numerous attempts have been made to switch immunosuppressive TAMs into an immunostimulatory type. Previously, we showed that a copper chelate, viz., copper N-(2-hydroxy acetophenone) glycinate [CuNG], can reprogram TAMs toward the proimmunogenic type to mount an antitumor immune response, but the underlying molecular mechanisms of skewing TAMs toward the proimmunogenic type remain elusive. Herein, we tried to explore the signaling mechanisms responsible for the reprogramming of TAMs. We observed that CuNG-induced ROS generation triggers activ...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5644043</comments>
            <pubDate>Wed, 25 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5644043</guid>        </item>
        <item>
            <title>Peritoneal macrophage from male and female SJL mice differ in IL-10 expression and macrophage maturation.</title>
            <link>http://www.medworm.com/index.php?rid=5626579&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262797%26dopt%3DAbstract</link>
            <description>Authors: Hussain S, Stohlman SA
    Abstract
    Injection of proteins and particulate antigens into the peritoneal cavity of male SJL mice preferentially activates T cells secreting Th2 cytokines. Identical immunizations of females activate T cells secreting Th1 cytokines. CD11b(+)F4/80(hi) LPM and CD11b(+)F4/80(lo) SPM populations were compared between naive males and females to define their role in supporting differential Th1 versus Th2 T cell activation. No sex-dependent differences in the expression of MHC class II, costimulatory molecules, and MR were detected. Immunization induced influx of CD11b(lo)F4/80(lo) cells in both sexes. CD11b(lo)F4/80(lo) cells consist predominantly of Ly6C(hi) monocytes, which mature into a Ly6C(-) SPM subset. Following immunization, equivalent frequencie...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5626579</comments>
            <pubDate>Wed, 18 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5626579</guid>        </item>
        <item>
            <title>Microenvironmental regulation of inducible nitric oxide synthase expression and nitric oxide production in mouse bone marrow-derived mast cells.</title>
            <link>http://www.medworm.com/index.php?rid=5626578&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262798%26dopt%3DAbstract</link>
            <description>Authors: Moon TC, Yoshimura T, Parsons T, Befus AD
    Abstract
    In addition to its well-known role in relaxation of vascular smooth muscle, NO modulates immune responses in a concentration- and location-specific manner. For MC, it is well accepted that exogenous NO regulates their function. However, there are inconsistencies in the literature of whether MC express NOS and make NO. MC progenitors mature in peripheral tissues, but the factors that influence MC maturation and their specific phenotype, such as whether they express NOS, are not well understood. To study microenvironmental conditions that could be &quot;permissive&quot; for NOS expression, we cultured BMMC in various conditions-BMMC(IL-3), BMMC(SCF/IL-3), or BMMC(SCF/IL-4)-for &amp;gt;3 weeks and examined NOS expression. We detected Nos2 ...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5626578</comments>
            <pubDate>Wed, 18 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5626578</guid>        </item>
        <item>
            <title>A novel p38-MAPK signaling axis modulates neutrophil biology in head and neck cancer.</title>
            <link>http://www.medworm.com/index.php?rid=5626577&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262799%26dopt%3DAbstract</link>
            <description>Authors: Dumitru CA, Fechner MK, Hoffmann TK, Lang S, Brandau S
    Abstract
    Neutrophils are emerging as important mediators in cancer progression. Recent studies associated neutrophils with poor clinical outcome of HNC patients and showed that HNC induces recruitment, survival, and release of proinflammatory factors by neutrophils in vitro. The molecular mechanisms through which HNC and other cancers modulate neutrophil biology are currently unknown. To explore these mechanisms, we used an in vitro system that models the interaction between human HNC cells and neutrophils or neutrophilic-differentiated HL-60 cells, respectively. We show that HNC-derived factors activate p38-MAPK in neutrophils, which partly promotes neutrophil survival, but not neutrophil recruitment and motility. Mos...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5626577</comments>
            <pubDate>Wed, 18 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5626577</guid>        </item>
        <item>
            <title>Donor- but not host-derived interleukin-10 contributes to the regulation of experimental graft-versus-host disease.</title>
            <link>http://www.medworm.com/index.php?rid=5626576&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262800%26dopt%3DAbstract</link>
            <description>Authors: Tawara I, Sun Y, Liu C, Toubai T, Nieves E, Evers R, Alrubaie M, Mathewson N, Tamaki H, Reddy P
    Abstract
    IL-10 is a key immune-regulatory cytokine, and its gene polymorphisms correlate with severity of clinical GVHD. IL-10 is made by a variety of donor and host cells, but the functional relevance of its source and its role in the biology of acute GVHD are not well understood. We used preclinical models to examine the relevance of IL-10(-/-) in donor and host cellular subsets on the severity of GVHD. IL-10(-/-) in host tissues or in the donor grafts did not alter donor Teff-mediated severity of GVHD. Furthermore, neither host-derived nor donor Teff-derived IL-10 was required for regulation of GVHD by WT CD4(+)CD25(+) donor Tregs. By contrast, Treg-derived IL-10, although no...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5626576</comments>
            <pubDate>Wed, 18 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5626576</guid>        </item>
        <item>
            <title>The role of the Src family kinase Lyn in the immunomodulatory activities of cathelicidin peptide LL-37 on monocytic cells.</title>
            <link>http://www.medworm.com/index.php?rid=5607223&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22246800%26dopt%3DAbstract</link>
            <description>Authors: Nijnik A, Pistolic J, Cho P, Filewod NC, Falsafi R, Ramin A, Harder KW, Hancock RE
    Abstract
    Cathelicidin LL-37 is a multifunctional, immunomodulatory and antimicrobial host-defense peptide of the human immune system. Here, we identified the role of SFKs in mediating the chemokine induction activity of LL-37 in monocytic cells. LL-37 induced SFK phosphorylation; and chemical inhibitors of SFKs suppressed chemokine production in response to LL-37 stimulation. SFKs were required for the downstream activation of AKT, but Ca(2+)-flux and MAPK induction were SFK-independent. Through systematic siRNA knockdown of SFK members, a requirement for Lyn in mediating LL-37 activity was identified. The involvement of Lyn in cathelicidin activities was further confirmed using Lyn-knockout...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5607223</comments>
            <pubDate>Fri, 13 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5607223</guid>        </item>
        <item>
            <title>Synergistic CD40 signaling on APCs and CD8 T cells drives efficient CD8 response and memory differentiation.</title>
            <link>http://www.medworm.com/index.php?rid=5607225&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22241832%26dopt%3DAbstract</link>
            <description>In this study, we address the exact role of CD40 expression on APCs and CD8 T cells using aCD40ab treatment in mice. We demonstrate that aCD40 antibodies have synergetic effects on APCs and CD8 T cells. Full efficiency of aCD40 treatment requires CD40 expression on both populations: if one of these cell populations is CD40-deficient, the CD8 T cell response is impaired. Most importantly, direct CD40 signaling on APCs and CD8 T cells affects CD8 T cell differentiation differently. In our model, CD40 expression on APCs plays an important but dispensable role on CD8 T cell expansion and effector functions during the early phase of the immune response. Conversely, CD40 on CD8 T cells is crucial and nonredundant for their progressive differentiation into memory cells. Altogether, these results ...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5607225</comments>
            <pubDate>Wed, 11 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5607225</guid>        </item>
        <item>
            <title>Sialoglycoproteins adsorbed by Pseudomonas aeruginosa facilitate their survival by impeding neutrophil extracellular trap through siglec-9.</title>
            <link>http://www.medworm.com/index.php?rid=5607224&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22241833%26dopt%3DAbstract</link>
            <description>Authors: Khatua B, Bhattacharya K, Mandal C
    Abstract
    PA is an opportunistic pathogen that is commonly associated with severe infection in immunocompromised hosts. Siglec-9 binds with Sias by cis interaction on the neutrophil surface, thereby reducing immunological activity. However, neutrophils bind with pathogens through trans interactions of siglec-9 with Sias. Neutrophils kill invading pathogens by NETs, along with extracellular phagocytosis. Here, we report the mode of the adsorption of Sias by PA from host serum, the interaction of PA(+Sias) with human neutrophils, and the resulting neutrophil immunological activity. The Î±2-3-linked sialoglycoproteins adsorbed by PA exhibited potent binding with the soluble siglec-9-Fc chimeras, CHO-siglec-9 and siglec-9 on neutrophils. The b...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5607224</comments>
            <pubDate>Wed, 11 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5607224</guid>        </item>
        <item>
            <title>Unusual timing of CD127 expression by mouse uterine natural killer cells.</title>
            <link>http://www.medworm.com/index.php?rid=5580206&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22227963%26dopt%3DAbstract</link>
            <description>Authors: Zhang J, Chen Z, Fritz JH, Rochman Y, Leonard WJ, Gommerman JL, Plumb AW, Abraham N, Croy BA
    Abstract
    Decidualization, a progesterone-dependent process that alters endometrial stromal cells at implantation sites in humans and rodents, is accompanied by a highly regulated, NK cell-dominated leukocyte influx into decidual basalis (DB). Whether uNK cells differentiate from uterine progenitor cells is unknown, as are the mechanisms restricting leukocytes to DB. We asked if cells expressing the early NK lineage marker CD127 (IL-7RÎ±) occurred in mouse decidua. CD127 was absent from gd6.5 decidual lymphoid cells but became expressed by a mature uNK cell subset in gd10.5 DB. DB and transient myometrial structures (MLAp) that ring maternal blood vessels supplying placentae express...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580206</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5580206</guid>        </item>
        <item>
            <title>Monocyte maturation, HIV susceptibility, and transmigration across the blood brain barrier are critical in HIV neuropathogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=5580205&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22227964%26dopt%3DAbstract</link>
            <description>Authors: Williams DW, Eugenin EA, Calderon TM, Berman JW
    Abstract
    HIV continues to be a global health crisis with more than 34 million people infected worldwide (UNAIDS: Report on the Global AIDS Epidemic 2010, Geneva, World Health Organization). HIV enters the CNS within 2 weeks of infection and establishes a spectrum of HAND in a large percentage of infected individuals. These neurologic deficits greatly impact the quality of life of those infected with HIV. The establishment of HAND is largely attributed to monocyte transmigration, particularly that of a mature CD14(+)CD16(+) monocyte population, which is more susceptible to HIV infection, across the BBB into the CNS parenchyma in response to chemotactic signals. To enter the CNS, junctional proteins on the monocytes must partic...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580205</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5580205</guid>        </item>
        <item>
            <title>Hypercholesterolemic LDL receptor-deficient mice mount a neutrophilic response to tuberculosis despite the timely expression of protective immunity.</title>
            <link>http://www.medworm.com/index.php?rid=5580204&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22227965%26dopt%3DAbstract</link>
            <description>We reported previously that host defense against Mtb was impaired by hypercholesterolemia in ApoE(-/-) mice, raising the possibility that people with HC could be more vulnerable to TB. The present study examined whether TB immunity was similarly impaired in a different hypercholesterolemic model, LDL-R(-/-) mice, which developed comparable elevation of total serum cholesterol as ApoE(-/-)mice when fed HC or LC diets. Like ApoE(-/-) mice, LDL-R(-/-) mice had an exaggerated lung inflammatory response to Mtb with increased tissue necrosis. Inflammation, foamy macrophage formation, and tissue necrosis in LDL-R(-/-) mice increased with the degree of hypercholesterolemia. Unlike ApoE(-/-) mice, LDL-R(-/-) mice fed a HC diet mounted a timely and protective adaptive immune response that restricted...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580204</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5580204</guid>        </item>
        <item>
            <title>Tissue stroma as a regulator of leukocyte recruitment in inflammation.</title>
            <link>http://www.medworm.com/index.php?rid=5580203&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22227966%26dopt%3DAbstract</link>
            <description>Authors: McGettrick HM, Butler LM, Buckley CD, Ed Rainger G, Nash GB
    Abstract
    The stromal milieu (cellular and matrix components) helps establish tissue &quot;address-codes&quot; that direct leukocyte behavior in inflamed tissue. Coordinated interactions among the stroma, leukocytes, and ECs dictate which leukocytes are recruited, whether they are retained within the inflamed site, and how long they survive. Herein, we discuss how the stromal milieu influences the leukocyte recruitment cascade. Moreover, we explore how corruption of the stromal phenotype in chronic inflammatory diseases contributes to undesired, continuous recruitment of leukocytes. Emerging complex, multicellular, multilayered (co-)culture models are now addressing the molecular circuitry involved in regulating stromal orga...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580203</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5580203</guid>        </item>
        <item>
            <title>Editorial: Semaphorins: a further chemotropic family expressed in the thymus.</title>
            <link>http://www.medworm.com/index.php?rid=5568615&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22215795%26dopt%3DAbstract</link>
            <description>Authors: Orciari S, Catalano A
    PMID: 22215795 [PubMed - in process] (Source: Journal of Leukocyte Biology)</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568615</comments>
            <pubDate>Sun, 01 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5568615</guid>        </item>
        <item>
            <title>Editorial: Molecular eavesdropping: phagocytic cells spy on bacterial communication.</title>
            <link>http://www.medworm.com/index.php?rid=5568614&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22215796%26dopt%3DAbstract</link>
            <description>Authors: HÃ¤nsch GM
    PMID: 22215796 [PubMed - in process] (Source: Journal of Leukocyte Biology)</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568614</comments>
            <pubDate>Sun, 01 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5568614</guid>        </item>
        <item>
            <title>Azithromycin drives in vitro GM-CSF/IL-4-induced differentiation of human blood monocytes toward dendritic-like cells with regulatory properties.</title>
            <link>http://www.medworm.com/index.php?rid=5538660&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22131344%26dopt%3DAbstract</link>
            <description>In conclusion, azithromycin modulates the differentiation of blood monocyte-derived DCs to form iA-DCs with a distinct phenotype similar to that of iMDCs, accompanied by enhanced phagocytic and efferocytic capabilities. It also modifies LPS-induced DC maturation by decreasing surface molecule expression required for T cell activation, increasing IL-10 production, and inducing MLR-reducing properties.
    PMID: 22131344 [PubMed - as supplied by publisher] (Source: Journal of Leukocyte Biology)</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538660</comments>
            <pubDate>Wed, 21 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538660</guid>        </item>
        <item>
            <title>Olfactomedin 4 defines a subset of human neutrophils.</title>
            <link>http://www.medworm.com/index.php?rid=5538645&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22187488%26dopt%3DAbstract</link>
            <description>Authors: Clemmensen SN, Bohr CT, RÃ¸rvig S, GlenthÃ¸j A, Mora-Jensen H, Cramer EP, Jacobsen LC, Larsen MT, Cowland JB, Tanassi JT, Heegaard NH, Wren JD, Silahtaroglu AN, Borregaard N
    Abstract
    OLFM4 was identified initially as a gene highly induced in myeloid stem cells by G-CSF treatment. A bioinformatics method using a global meta-analysis of microarray data predicted that OLFM4 would be associated with specific granules in human neutrophils. Subcellular fractionation of peripheral blood neutrophils demonstrated complete colocalization of OLFM4 with the specific granule protein NGAL, and stimulation of neutrophils with PMA resulted in corelease of NGAL and OLFM4, proving that OLFM4 is a genuine constituent of neutrophil-specific granules. In accordance with this, OLFM4 mRNA peaked...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538645</comments>
            <pubDate>Tue, 20 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538645</guid>        </item>
        <item>
            <title>K12/SECTM1, an interferon-Î³ regulated molecule, synergizes with CD28 to costimulate human T cell proliferation.</title>
            <link>http://www.medworm.com/index.php?rid=5538647&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22184754%26dopt%3DAbstract</link>
            <description>Authors: Wang T, Huang C, Lopez-Coral A, Slentz-Kesler KA, Xiao M, Wherry EJ, Kaufman RE
    Abstract
    CD7 is a cell-surface molecule, expressed on T lymphocytes and NK cells, which functions as a costimulatory receptor for T cell proliferation. SECTM1 has been proposed as a ligand for CD7. However, the expression pattern of this molecule in human immune cells and role in human T cell function remain unclear. In the present study, using human rSECTM1, we demonstrate that SECTM1 strongly costimulates CD4 and CD8 T cell proliferation and induces IFN-Î³ production, likely via a CD7-dependent mechanism. In addition, SECTM1 synergizes with suboptimal anti-CD28 to strongly augment T cell functions. We found a robust induction of IL-2 production when SECTM1 and anti-CD28 signals were present w...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538647</comments>
            <pubDate>Mon, 19 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538647</guid>        </item>
        <item>
            <title>Inhibition of NADPH oxidase activation by peptides mapping within the dehydrogenase region of Nox2-A &quot;peptide walking&quot; study.</title>
            <link>http://www.medworm.com/index.php?rid=5538646&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22184755%26dopt%3DAbstract</link>
            <description>In this study, the &quot;peptide walking&quot; approach was applied to the DH region of Nox2 (residues 288-570) with the purpose of identifying domains of functional importance in the assembly and/or catalytic function of the NADPH oxidase complex of phagocytes. Ninety-one overlapping 15-mer peptides were synthesized to cover the full length of the Nox2 DH region, and these were tested for the ability to interfere with the activation of the oxidase in vitro in two semirecombinant cell-free systems. The first consisted of phagocyte membranes p47(phox), p67(phox), and Rac1 and an amphiphile; the second was p47(phox)- and amphiphile-free and contained prenylated Rac1. We identified 10 clusters of inhibitory peptides with IC(50) values of 10 Î¼M, all of which were inhibitory, also in the absence of p47(...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538646</comments>
            <pubDate>Mon, 19 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538646</guid>        </item>
        <item>
            <title>Role of IFN-Î³ in the establishment of anterior chamber-associated immune deviation (ACAID)-induced CD8+ T regulatory cells.</title>
            <link>http://www.medworm.com/index.php?rid=5538648&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22180630%26dopt%3DAbstract</link>
            <description>This study tested the hypothesis that IFN-Î³ is needed for alloantigen-specific ACAID CD8(+) Tregs to execute their suppressive function but is not required for the establishment of ACAID CD8(+) Tregs. To address this hypothesis, ACAID was induced by injecting BALB/c spleen cells into the AC of WT C57BL/6 mice, IFN-Î³(-/-) C57BL/6 mice, or anti-IFN-Î³-treated WT C57BL/6 mice. LAT assays using C57BL/6 APCs as stimulators, CD4(+) T cells from C57BL/6 mice previously immunized toward BALB/c alloantigens as effector cells, and IFN-Î³-competent, IFN-Î³(-/-), or IFN-Î³R(-/-) CD8(+) Tregs were used to evaluate the suppressive function of CD8(+) ACAID Tregs in response to IFN-Î³. IFN-Î³(-/-) mice or mice treated with anti-IFN-Î³ antibody prior to AC injection of alloantigen failed to develop ACAID...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538648</comments>
            <pubDate>Fri, 16 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538648</guid>        </item>
        <item>
            <title>M-ficolin and leukosialin (CD43): new partners in neutrophil adhesion.</title>
            <link>http://www.medworm.com/index.php?rid=5538651&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22167719%26dopt%3DAbstract</link>
            <description>Authors: Moreno-Amaral AN, Gout E, Danella-Polli C, Tabarin F, Lesavre P, Pereira-da-Silva G, Thielens NM, Halbwachs-Mecarelli L
    Abstract
    M-ficolin specificity for sialylated ligands prompted us to investigate its interactions with the main membrane sialoprotein of human neutrophils, CD43. rM-ficolin bound CD43 and prevented the access of anti-CD43 mAb. Moreover, rM-ficolin reacted exclusively with CD43 on Western blots of neutrophil lysate. We confirmed that M-ficolin is secreted by fMLP-activated neutrophils, and this endogenous M-ficolin also binds to CD43 and competes with anti-CD43 mAb. Anti-CD43 antibody cross-linking or fMLP resulted in M-ficolin and CD43 colocalization on polarized neutrophils. The binding of rM-ficolin to resting neutrophils induced cell polarization, adhe...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538651</comments>
            <pubDate>Tue, 13 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538651</guid>        </item>
        <item>
            <title>Cell type- and stimulus-specific mechanisms for post-transcriptional control of neutrophil chemokine gene expression.</title>
            <link>http://www.medworm.com/index.php?rid=5538650&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22167720%26dopt%3DAbstract</link>
            <description>Authors: Hamilton T, Li X, Novotny M, Pavicic PG, Datta S, Zhao C, Hartupee J, Sun D
    Abstract
    mRNAs encoding inflammatory chemokines that recruit neutrophils frequently exhibit short half-lives that serve to limit their expression under inappropriate conditions but are often prolonged to ensure adequate levels during inflammatory response. Extracellular stimuli that modulate the stability of such mRNAs may be the same as the transcriptional activator, as is the case with TLR ligands, or may cooperate with independent transcriptional stimuli, as with IL-17, which extends the half-life of TNF-induced transcripts. These different stimuli engage independent signaling pathways that target different instability mechanisms distinguished by dependence on different regulatory nucleotide seq...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538650</comments>
            <pubDate>Tue, 13 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538650</guid>        </item>
        <item>
            <title>Galectin-1 and -3 gene silencing in immature and mature dendritic cells enhances T cell activation and interferon-Î³ production.</title>
            <link>http://www.medworm.com/index.php?rid=5538649&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22167721%26dopt%3DAbstract</link>
            <description>Authors: Mobergslien A, Sioud M
    Abstract
    DCs are specialized APCs capable of inducing T cell activation as well as promoting tolerance. Although Gal, a family of Î²-galactoside-binding proteins, were found to affect immunity, little is known about the contribution of DC-expressed Gal on T cell activation. Here, we show that human imDCs and mDCs constitutively express Gal-1, Gal-3, Gal-8, and Gal-9 at mRNA and protein levels. Two of the most abundant Gal-Gal-1 and Gal-3-were highly expressed and detected on the cell surface of DCs. In contrast to Gal-8, knockdown of Gal-1 or Gal-3 in DCs enhanced allogeneic T cell responses. This was observed with imDCs and mDCs, but the effects were more pronounced with imDCs. Furthermore, allogeneic CD4(+) T cells incubated with Gal-1 or Gal-3 kno...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538649</comments>
            <pubDate>Tue, 13 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538649</guid>        </item>
        <item>
            <title>Rv2468c, a novel Mycobacterium tuberculosis protein that costimulates human CD4+ T cells through VLA-5.</title>
            <link>http://www.medworm.com/index.php?rid=5538652&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22158781%26dopt%3DAbstract</link>
            <description>Authors: Li Q, Ding X, Thomas JJ, Harding CV, Pecora ND, Ziady AG, Shank S, Boom WH, Lancioni CL, Rojas RE
    Abstract
    Mtb regulates many aspects of the host immune response, including CD4(+) T lymphocyte responses that are essential for protective immunity to Mtb, and Mtb effects on the immune system are paradoxical, having the capacity to inhibit (immune evasion) and to activate (adjuvant effect) immune cells. Mtb regulates CD4(+) T cells indirectly (e.g., by manipulation of APC function) and directly, via integrins and TLRs expressed on T cells. We now report that previously uncharacterized Mtb protein Rv2468c/MT2543 can directly regulate human CD4(+) T cell activation by delivering costimulatory signals. When combined with TCR stimulation (e.g., anti-CD3), Rv2468c functioned as a ...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538652</comments>
            <pubDate>Wed, 07 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538652</guid>        </item>
        <item>
            <title>Dendritic cell-associated lectin 2 (DCAL2) defines a distinct CD8Î±-dendritic cell subset.</title>
            <link>http://www.medworm.com/index.php?rid=5538653&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22147811%26dopt%3DAbstract</link>
            <description>Authors: Kasahara S, Clark EA
    Abstract
    CLRs on DCs play important roles in immunity and are expressed selectively on certain DC subsets. Murine DCAL2 (myeloid inhibitory C-type lectin/Clec12a) is a type-II CLR with an ITIM. Using a mouse DCAL2-specific mAb, we found that DCAL2 is expressed at relatively high levels on APCs and that DCAL2 expression can be used to divide CD8Î±(-) DCs into DCAL2(+)DCIR2(-) and DCAL2(-)DCIR2(+) subpopulations. CD8Î±(-)DCAL2(+) DC, CD8Î±(-)DCIR2(+) DC, and CD8Î±(+)DCAL2(+) DC subsets each express different levels of TLRs and respond to unique classes of TLR ligands by producing distinct sets of cytokines. Whereas CD8Î±(-)DCAL2(+) DCs robustly produce cytokines, including IL-12, in response to CpG, CD8Î±(-)DCIR2(+) DCs produce only TNF-Î± and IL-10 in m...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538653</comments>
            <pubDate>Tue, 06 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538653</guid>        </item>
        <item>
            <title>The monomer-dimer equilibrium and glycosaminoglycan interactions of chemokine CXCL8 regulate tissue-specific neutrophil recruitment.</title>
            <link>http://www.medworm.com/index.php?rid=5538655&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22140266%26dopt%3DAbstract</link>
            <description>In this study, we show that monomers and dimers are also active in the mouse peritoneum but that the role of monomer-dimer equilibrium is distinctly different between these tissues and that mutations in GAG-binding residues render CXCL8 less active in the peritoneum but more active in the lung. We propose that tissue-specific differences in chemokine gradient formation, resulting from tissue-specific differences in GAG interactions, are responsible for the observed differences in neutrophil recruitment. Our observation of differential roles played by the CXCL8 monomer-dimer equilibrium and GAG interactions in different tissues is novel and reveals an additional level of complexity of how chemokine dimerization regulates in vivo recruitment.
    PMID: 22140266 [PubMed - as supplied by publi...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538655</comments>
            <pubDate>Fri, 02 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538655</guid>        </item>
        <item>
            <title>IL-10-induced gp130 expression in mouse mast cells permits IL-6 trans-signaling.</title>
            <link>http://www.medworm.com/index.php?rid=5538654&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22140267%26dopt%3DAbstract</link>
            <description>This study identifies factors that regulate mouse mast cell gp130 expression and signaling and makes conspicuous the limitations of using cultured mouse mast cells to study the effects of the IL-6/IL-12 cytokine family on mast cell biology.
    PMID: 22140267 [PubMed - as supplied by publisher] (Source: Journal of Leukocyte Biology)</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538654</comments>
            <pubDate>Fri, 02 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538654</guid>        </item>
        <item>
            <title>Editorial: An apple a day keeps colitis away.</title>
            <link>http://www.medworm.com/index.php?rid=5538657&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22131358%26dopt%3DAbstract</link>
            <description>Authors: Hofseth LJ, Matesic LE
    PMID: 22131358 [PubMed - in process] (Source: Journal of Leukocyte Biology)</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538657</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538657</guid>        </item>
        <item>
            <title>Editorial: Will the real neutrophil please stand up?</title>
            <link>http://www.medworm.com/index.php?rid=5538656&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22131359%26dopt%3DAbstract</link>
            <description>Authors: Zarember KA, Kuhns DB
    PMID: 22131359 [PubMed - in process] (Source: Journal of Leukocyte Biology)</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538656</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538656</guid>        </item>
        <item>
            <title>Cell-surface receptors on macrophages and dendritic cells for attachment and entry of influenza virus.</title>
            <link>http://www.medworm.com/index.php?rid=5538663&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22124137%26dopt%3DAbstract</link>
            <description>Authors: Londrigan SL, Tate MD, Brooks AG, Reading PC
    Abstract
    Airway MÎ¦ and DCs are important components of innate host defense and can play a critical role in limiting the severity of influenza virus infection. Although it has been well established that cell-surface SA acts as a primary attachment receptor for IAV, the particular receptor(s) or coreceptor(s) that mediate IAV entry into any cell, including MÎ¦ and DC, have not been clearly defined. Identifying which receptors are involved in attachment and entry of IAV into immune cells may have important implications in regard to understanding IAV tropism and pathogenesis. Recent evidence suggests that specialized receptors on MÎ¦ and DCs, namely CLRs, can act as capture and/or entry receptors for many viral pathogens, including...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538663</comments>
            <pubDate>Wed, 30 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538663</guid>        </item>
        <item>
            <title>Stimulation of Ly-6G on neutrophils in LPS-primed mice induces platelet-activating factor (PAF)-mediated anaphylaxis-like shock.</title>
            <link>http://www.medworm.com/index.php?rid=5538661&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22131343%26dopt%3DAbstract</link>
            <description>Authors: Tanaka Y, Nagai Y, Kuroishi T, Endo Y, Sugawara S
    Abstract
    Previously, two anti-Ly-6G mAb-RB6-8C5 and 1A8-have been used to deplete neutrophils in mice and to clarify their involvement in immune responses. During the course of experiments on neutrophil depletion, we noticed that i.v. injection of RB6-8C5 or 1A8 induced anaphylaxis-like shock in mice pretreated i.v. with LPS. Signs of shock, such as hypothermia, appeared within a few minutes, and the mice died of shock within 20 min of the antibody injection. In vivo experiments, including depletion of various cell types, indicated that neutrophils and macrophages (but not platelets, basophils, or mast cells) are involved in the shock. Experiments using various drugs and gene-targeted mice demonstrated that PAF is the centr...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538661</comments>
            <pubDate>Wed, 30 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538661</guid>        </item>
        <item>
            <title>Myeloperoxidase associated with neutrophil extracellular traps is active and mediates bacterial killing in the presence of hydrogen peroxide.</title>
            <link>http://www.medworm.com/index.php?rid=5538659&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22131345%26dopt%3DAbstract</link>
            <description>The objective of this study was to establish whether MPO associated with NETs is active and able to kill bacteria. Neutrophils were stimulated with PMA to release NETs. Peroxidase activity measurements were performed and showed that enzymatically active MPO was released from the neutrophils, 2-4 h after stimulation, concomitant with NET formation. Approximately 30% of the total cellular MPO was released, with the majority bound to the NETs. The bound enzyme retained its activity. Staphylococcus aureus were not killed when added to preformed NETs under our assay conditions. However, addition of H(2)O(2) to the bacteria in the presence of NETs resulted in MPO-dependent killing, which was observed with NETs in situ and with NETs when they were removed from the neutrophils by limited DNase dig...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538659</comments>
            <pubDate>Wed, 30 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538659</guid>        </item>
        <item>
            <title>Mechanisms of sex disparities in influenza pathogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=5538658&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22131346%26dopt%3DAbstract</link>
            <description>Authors: Klein SL, Hodgson A, Robinson DP
    Abstract
    Epidemiological evidence from influenza outbreaks and pandemics reveals that morbidity and mortality are often higher for women than men. Sex differences in the outcome of influenza are age-dependent, often being most pronounced among adults of reproductive ages (18-49 years of age) and sometimes reflecting the unique state of pregnancy in females, which is a risk factor for severe disease. Small animal models of influenza virus infection illustrate that inflammatory immune responses also differ between the sexes and impact the outcome of infection, with females generating higher proinflammatory cytokine and chemokine responses and experiencing greater morbidity and mortality than males. Males and females also respond differently t...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538658</comments>
            <pubDate>Wed, 30 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538658</guid>        </item>
        <item>
            <title>Histone deacetylase inhibitors impair NK cell viability and effector functions through inhibition of activation and receptor expression.</title>
            <link>http://www.medworm.com/index.php?rid=5538664&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22124136%26dopt%3DAbstract</link>
            <description>Authors: Rossi LE, Avila DE, Spallanzani RG, Ziblat A, Fuertes MB, Lapyckyj L, Croci DO, Rabinovich GA, Domaica CI, Zwirner NW
    Abstract
    HDACi are being used as a novel, therapeutic approach for leukemias and other hematological malignancies. However, their effect on immune cells remains ill-defined, as HDACi may impair immune surveillance. In this work, we demonstrate that TSA, VPA, and NaB inhibited IFN-Î³ production by CD56(dim) and CD56(bright) NK cells and NK cell-mediated cytotoxicity against K562 target cells. HDACi promoted minor NK cell apoptosis but inhibited nuclear mobilization of NF-ÎºB p50, which was accompanied by a robust down-regulation of NKG2D and NKp46 on resting NK cells and of NKG2D, NKp44, NKp46, and CD25 on cytokine-activated NK cells. Decreased CD25 expressi...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538664</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538664</guid>        </item>
        <item>
            <title>Non-human primate dendritic cells.</title>
            <link>http://www.medworm.com/index.php?rid=5538662&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22124138%26dopt%3DAbstract</link>
            <description>Authors: Jesudason S, Collins MG, Rogers NM, Kireta S, Coates PT
    Abstract
    Non-human primates (NHP) are essential translational models for biomedical research. Dendritic cells (DC) are a group of antigen presenting cells that play pivotal roles in the immunobiology of health and disease and are attractive cells for adoptive immunotherapy to stimulate and suppress immunity. DC have been studied extensively in humans and mice but until recently, have not been well characterized in NHP. This review considers the available data about DC across a range of NHP species and summarizes the understanding of in vitro-propagated DC and in vivo-isolated DC, which is now established. It is clear that although NHP DC exist within the paradigm of human DC, there are important functional and phenoty...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538662</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538662</guid>        </item>
        <item>
            <title>Impaired function of Fanconi anemia type C-deficient macrophages.</title>
            <link>http://www.medworm.com/index.php?rid=5538665&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22106009%26dopt%3DAbstract</link>
            <description>Authors: Liu Y, Ballman K, Li D, Khan S, Derr-Yellin E, Shou W, Haneline LS
    Abstract
    FA is a genetic disorder characterized by BM failure, developmental defects, and cancer predisposition. Previous studies suggest that FA patients exhibit alterations in immunologic function. However, it is unclear whether the defects are immune cell-autonomous or secondary to leukopenia from evolving BM failure. Given the central role that macrophages have in the innate immune response, inflammation resolution, and antigen presentation for acquired immunity, we examined whether macrophages from Fancc-/- mice exhibit impaired function. Peritoneal inflammation induced by LPS or sodium periodate resulted in reduced monocyte/macrophage recruitment in Fancc-/- mice compared with WT controls. Fancc-/- mi...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538665</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538665</guid>        </item>
        <item>
            <title>Neutrophil-derived matrix metalloproteinase-9 is a potent activator of trypsinogen in acinar cells in acute pancreatitis.</title>
            <link>http://www.medworm.com/index.php?rid=5538666&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22100390%26dopt%3DAbstract</link>
            <description>Authors: Awla D, Abdulla A, Syk I, Jeppsson B, RegnÃ©r S, Thorlacius H
    Abstract
    MMPs are generally considered to regulate degradation and remodeling of the ECM. Convincing data also implicate a role for MMPs in inflammatory conditions, such as AP, although the mechanisms are not known. The aim of this study was to define the role of MMPs in regulating activation of trypsinogen and tissue damage in AP, which was induced by infusion of taurocholate into the pancreatic duct in mice. A broad-spectrum MMP inhibitor (BB-94) and MMP-9 gene-deficient mice were used. Neutrophil secretions and rMMP-9 were used to stimulate trypsinogen activation in isolated acinar cells. Taurocholate challenge increased serum amylase, neutrophil infiltration, MIP-2 (CXCL2) formation, trypsinogen activation, ...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538666</comments>
            <pubDate>Fri, 18 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538666</guid>        </item>
        <item>
            <title>Technical Advance: In vitro production of distinct dendritic-like antigen-presenting cells from self-renewing hematopoietic stem cells.</title>
            <link>http://www.medworm.com/index.php?rid=5427983&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22075929%26dopt%3DAbstract</link>
            <description>Authors: Hinton RA, O'Neill HC
    Abstract
    A novel CD11c(lo)CD11b(hi)MHC-II(-)CD8Î±(-) dendritic-like cell (L-DC) develops in cocultures of bone marrow over splenic stroma. L-DCs are distinct from other DC subsets and have potential importance in spleen for immunity to blood-borne antigens. As production is maintained in cultures for &amp;gt;12 months, L-DC development evidently depends on self-renewing progenitors. To improve this culture system, highly purified HSCs were sorted from bone marrow and used to establish cocultures. Nonadherent cells produced were analyzed for surface marker expression and capacity to activate/inhibit T cells. Cocultures produced a pure population of L-DCs for up to 12 months, which were strong activators of CD8(+) T cells. The in vitro production of a pure ...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5427983</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5427983</guid>        </item>
        <item>
            <title>Strain-dependent induction of neutrophil histamine production and cell death by Pseudomonas aeruginosa.</title>
            <link>http://www.medworm.com/index.php?rid=5427984&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22075928%26dopt%3DAbstract</link>
            <description>Authors: Xu X, Zhang H, Song Y, Lynch SV, Lowell CA, Wiener-Kronish JP, Caughey GH
    Abstract
    Airway diseases often feature persistent neutrophilic inflammation and infection. In cystic fibrosis bronchitis, for example, Pseudomonas aeruginosa is isolated frequently. Previously, this laboratory revealed that neutrophils become major sources of histamine in mice with tracheobronchitis caused by the wall-less bacterium Mycoplasma pulmonis. To test the hypothesis that more-broadly pathogenic P. aeruginosa (which expresses cell wall-associated LPS and novel toxins) has similar effects, we incubated naÃ¯ve mouse neutrophils with two strains of P. aeruginosa. Strain PAO1 greatly increased neutrophil histamine content and secretion, whereas strain PA103 depressed histamine production by kill...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5427984</comments>
            <pubDate>Thu, 10 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5427984</guid>        </item>
        <item>
            <title>Macrophage-elicited osteoclastogenesis in response to Brucella abortus infection requires TLR2/MyD88-dependent TNF-Î± production.</title>
            <link>http://www.medworm.com/index.php?rid=5427982&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22075930%26dopt%3DAbstract</link>
            <description>Authors: Delpino MV, Barrionuevo P, Macedo GC, Oliveira SC, Di Genaro S, Scian R, Miraglia MC, Fossati CA, Baldi PC, Giambartolomei GH
    Abstract
    Osteoarticular complications are common in human brucellosis, but the pathogenic mechanisms involved are largely unknown. In this manuscript, we described an immune mechanism for inflammatory bone loss in response to infection by Brucella abortus. We established a requirement for MyD88 and TLR2 in TNF-Î±-elicited osteoclastogenesis in response to B. abortus infection. CS from macrophages infected with B. abortus induced BMM to undergo osteoclastogenesis. Although B. abortus-infected macrophages actively secreted IL-1Î², IL-6, and TNF-Î±, osteoclastogenesis depended on TNF-Î±, as CS from B. abortus-infected macrophages failed to induce osteo...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5427982</comments>
            <pubDate>Thu, 10 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5427982</guid>        </item>
        <item>
            <title>Pivotal Advance: Peritoneal cavity B-1 B cells have phagocytic and microbicidal capacities and present phagocytosed antigen to CD4+ T cells.</title>
            <link>http://www.medworm.com/index.php?rid=5427989&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22058420%26dopt%3DAbstract</link>
            <description>Authors: Parra D, Rieger AM, Li J, Zhang YA, Randall LM, Hunter CA, Barreda DR, Sunyer JO
    Abstract
    Breaking the long-held paradigm that primary B cells are not phagocytic, several studies have demonstrated recently that B cells from fish, amphibians, and reptilians have a significant phagocytic capacity. Whether such capacity has remained conserved in certain mammalian B cell subsets is presently an enigma. Here, we report a previously unrecognized ability of PerC B-1a and B-1b lymphocytes to phagocytose latex beads and bacteria. In contrast, B-2 lymphocytes had an almost negligible ability to internalize these particles. Upon phagocytosis, B-1a and B-1b cells were able to mature their phagosomes into phagolysosomes and displayed the ability to kill internalized bacteria. Important...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5427989</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5427989</guid>        </item>
        <item>
            <title>Lipid-cytokine-chemokine cascades orchestrate leukocyte recruitment in inflammation.</title>
            <link>http://www.medworm.com/index.php?rid=5427988&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22058421%26dopt%3DAbstract</link>
            <description>Authors: Sadik CD, Luster AD
    Abstract
    Chemoattractants are pivotal mediators of host defense, orchestrating the recruitment of immune cells into sites of infection and inflammation. Chemoattractants display vast chemical diversity and include bioactive lipids, proteolytic fragments of serum proteins, and chemokines (chemotactic cytokines). All chemoattractants induce chemotaxis by activating seven-transmembrane-spanning GPCRs expressed on immune cells, establishing the concept that all chemoattractants are related in function. However, although chemoattractants have overlapping functions in vitro, recent in vivo data have revealed that they function, in many cases, nonredundantly in vivo. The chemically diverse nature of chemoattractants contributes to the fine control of leukocyte...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5427988</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5427988</guid>        </item>
        <item>
            <title>TLR9 and TLR7 agonists mediate distinct type I IFN responses in humans and nonhuman primates in vitro and in vivo.</title>
            <link>http://www.medworm.com/index.php?rid=5427987&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22058422%26dopt%3DAbstract</link>
            <description>This study used new PCR arrays that selectively amplify individual I-IFN subtype genes of human and nonhuman primates to characterize the TLR7- and -9-mediated IFN response in vitro and in vivo. We show that in human PBMCs, TLR7 agonists induce a rapid burst of I-IFN transcripts, consisting primarily of IFN-Î±1/13, -Î±2, and -Î±14. In contrast, TLR9 agonists, regardless of the type used (CpG C-, B-, or D-ODN), prompted slower but sustained expression of IFN-Î±1/13, -Î±2, -Î±7, -Î±8, -Î±10, -Î±14, -Î±16, and -Î±21. These qualitative differences were translated downstream as differences in the pattern of IFN-inducible genes. In macaque PBMCs, imiquimod produced a short burst of IFN mRNA, dominated by IFN-Î±8, whereas C- or D-ODN induced a greater than tenfold increase in transcripts for all ...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5427987</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5427987</guid>        </item>
        <item>
            <title>Pivotal Advance: Characterization of mouse liver phagocytic B cells in innate immunity.</title>
            <link>http://www.medworm.com/index.php?rid=5427986&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22058423%26dopt%3DAbstract</link>
            <description>Authors: Nakashima M, Kinoshita M, Nakashima H, Habu Y, Miyazaki H, Shono S, Hiroi S, Shinomiya N, Nakanishi K, Seki S
    Abstract
    Although B cells in vertebrates have been thought to lack phagocytic activity, there has been a recent report of such ability by the B cells of early vertebrates such as fish and frogs. Here, we show for the first time that mouse liver IgM(+) B cells actively phagocytose microsphere beads and Escherichia coli and that they effectively kill bacterial cells. Such phagocytic activity is not observed in other liver MNCs, except for F4/80(+) Kupffer cells. In the presence of fresh mouse serum (but not heat-inactivated serum), the heat-killed E. coli phagocytic activity of liver B cells increased significantly but was inhibited significantly by anticomplement co...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5427986</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5427986</guid>        </item>
        <item>
            <title>Natural killer cell-produced IFN-Î³ and TNF-Î± induce target cell cytolysis through up-regulation of ICAM-1.</title>
            <link>http://www.medworm.com/index.php?rid=5383319&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22045868%26dopt%3DAbstract</link>
            <description>Authors: Wang R, Jaw JJ, Stutzman NC, Zou Z, Sun PD
    Abstract
    NK cells control tumor and virus-infected cells through releasing cytotoxic granules and proinflammatory cytokines. IFN-Î³ and TNF-Î± secretions and cytotoxicity are regarded as two distinct functions of NK cells with little synergy in between as results of early association of the two functions with distinct subsets of NK populations and of the studies showing target cells developing NK resistance upon IFN-Î³ treatment. Here, we show that IFN-Î³ and TNF-Î± synergistically enhance NK cell cytotoxicity through NF-ÎºB-dependent up-regulation of ICAM-1 expression in target cells, thereby promoting their conjugate formation with NK cells. Neutralizing IFN-Î³ and TNF-Î± during cytolysis significantly impaired NK cell lysis of ...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383319</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383319</guid>        </item>
        <item>
            <title>IL-27 inhibits pathophysiological intraocular neovascularization due to laser burn.</title>
            <link>http://www.medworm.com/index.php?rid=5383318&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22045869%26dopt%3DAbstract</link>
            <description>Authors: Hasegawa E, Oshima Y, Takeda A, Saeki K, Yoshida H, Sonoda KH, Ishibashi T
    Abstract
    AMD is the most common disease leading to acquired blindness in developed countries. CNV is the foremost cause of AMD and is thought to be induced by regional inflammation as a result of age-related conformational changes of the chorioretinal interface. Here, we show that IL-27, a member of the IL-6/IL-12 cytokine family, has an angiostatic effect and regulates the development of laser-induced experimental CNV in mice. In this model, IL-27 expression increased in the damaged choroid and peaked at the 24th-time-point. IL-27 neutralization, induced by inoculating an antagonistic antibody into the vitreous cavity, enhanced VEGF production and the extent of CNV. By contrast, the administration ...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383318</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383318</guid>        </item>
        <item>
            <title>Transcriptional activation of the IL31 gene by NFAT and STAT6.</title>
            <link>http://www.medworm.com/index.php?rid=5383317&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22045870%26dopt%3DAbstract</link>
            <description>In this study, we investigated how expression of IL-31 is regulated in T cells and mast cells. We observed that expression of IL-31 required a calcium signal and was dependent on the calcineurin-NFAT signaling pathway. Moreover, we found that IL-31 promoter contains a positive regulatory region that mediates calcium- and IL-4-dependent induction of the IL-31 gene and demonstrated that a change into an open chromatin conformation occurs in this region after stimulation with calcium and IL-4. Whereas IL-4 responsiveness required STAT6 binding sites, calcium responsiveness of IL-31 promoter required NFAT binding sites that bind NFATc1 and NFATc2 in vitro and in vivo. The induction of IL-31 promoter activity was impaired when these sites were mutated but was enhanced by CA-NFATc1 or STAT6 prot...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383317</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383317</guid>        </item>
        <item>
            <title>Editorial: Switching on arginase in M2 macrophages.</title>
            <link>http://www.medworm.com/index.php?rid=5383316&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22045920%26dopt%3DAbstract</link>
            <description>Authors: Briken V, Mosser DM
    PMID: 22045920 [PubMed - in process] (Source: Journal of Leukocyte Biology)</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383316</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383316</guid>        </item>
        <item>
            <title>Editorial: Neutrophil apoptosis: hot on the TRAIL of inflammatory resolution.</title>
            <link>http://www.medworm.com/index.php?rid=5383315&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22045921%26dopt%3DAbstract</link>
            <description>Authors: Leitch AE, Lucas CD, Rossi AG
    PMID: 22045921 [PubMed - in process] (Source: Journal of Leukocyte Biology)</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383315</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383315</guid>        </item>
        <item>
            <title>The impact of aging on memory T cell phenotype and function in the human bone marrow.</title>
            <link>http://www.medworm.com/index.php?rid=5383328&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22013229%26dopt%3DAbstract</link>
            <description>Authors: Herndler-Brandstetter D, Landgraf K, Tzankov A, Jenewein B, Brunauer R, Laschober GT, Parson W, Kloss F, Gassner R, Lepperdinger G, Grubeck-Loebenstein B
    Abstract
    Recently, the BM has been shown to play a key role in regulating the survival and function of memory T cells. However, the impact of aging on these processes has not yet been studied. We demonstrate that the number of CD4(+) and CD8(+) T cells in the BM is maintained during aging. However, the composition of the T cell pool in the aged BM is altered with a decline of naÃ¯ve and an increase in T(EM) cells. In contrast to the PB, a highly activated CD8(+)CD28(-) T cell population, which lacks the late differentiation marker CD57, accumulates in the BM of elderly persons. IL-6 and IL-15, which are both increased in ...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383328</comments>
            <pubDate>Tue, 25 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383328</guid>        </item>
        <item>
            <title>Histone deacetylase inhibition facilitates GM-CSF-mediated expansion of myeloid-derived suppressor cells in vitro and in vivo.</title>
            <link>http://www.medworm.com/index.php?rid=5383326&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22028329%26dopt%3DAbstract</link>
            <description>Authors: Rosborough BR, Castellaneta A, Natarajan S, Thomson AW, Turnquist HR
    Abstract
    Chromatin-modifying HDACi exhibit anti-inflammatory properties that reflect their ability to suppress DC function and enhance regulatory T cells. The influence of HDACi on MDSCs, an emerging regulatory leukocyte population that potently inhibits T cell proliferation, has not been examined. Exposure of GM-CSF-stimulated murine BM cells to HDACi led to a robust expansion of monocytic MDSC (CD11b(+)Ly6C(+)F4/80(int)CD115(+)), which suppressed allogeneic T cell proliferation in a NOS- and HO-1-dependent manner with similar potency to control MDSCs. The increased yield of MDSCs correlated with blocked differentiation of BM cells and an overall increase in HSPCs (Lin(-)Sca-1(+)c-Kit(+)). In vivo, TSA e...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383326</comments>
            <pubDate>Tue, 25 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383326</guid>        </item>
        <item>
            <title>Glucocorticoids inhibit dendritic cell maturation induced by Toll-like receptor 7 and Toll-like receptor 8.</title>
            <link>http://www.medworm.com/index.php?rid=5383325&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22028330%26dopt%3DAbstract</link>
            <description>Authors: LarangÃ© A, Antonios D, Pallardy M, Kerdine-RÃ¶mer S
    Abstract
    GCs are widely prescribed to treat inflammatory disorders and autoimmune and allergic diseases. Their anti-inflammatory and immunosuppressive effects may be related, in part, to their ability to control the maturation and functions of DCs. Here, we report that GCs inhibit the maturation of human CD34-DCs induced by the TLR7 agonist imiquimod and the TLR8 agonist 3M-002. GCs down-regulate the expression of CD86, CD40, CD83, CCR7, and HLA-DR on DCs and inhibit IL-6 and IL-12p40 production by DCs following TLR7 and TLR8 stimulation. This inhibitory effect is abolished by RU486, suggesting a role for GR transcriptional activity. Our results also show that GCs do not affect TLR-mediated DNA-binding activity of NF-ÎºB...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383325</comments>
            <pubDate>Tue, 25 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383325</guid>        </item>
        <item>
            <title>The emerging role of leukocyte immunoglobulin-like receptors (LILRs) in HIV-1 infection.</title>
            <link>http://www.medworm.com/index.php?rid=5383324&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22028331%26dopt%3DAbstract</link>
            <description>Authors: Lichterfeld M, Yu XG
    Abstract
    LILRs represent a group of immunomodulatory molecules that regulate the functional properties of professional APCs and influence immune activation in a variety of disease contexts. Many members of the LILR family recognize peptide/MHC class I complexes as their physiological ligands, and increasing evidence suggests that such interactions are prominently influenced by polymorphisms in HLA class I alleles or sequence variations in the presented antigenic peptides. Emerging data show that LILRs are involved in multiple, different aspects of HIV-1 disease pathogenesis and may critically influence spontaneous HIV-1 disease progression. Here, we review recent progress in understanding the role of LILR during HIV-1 infection by focusing on the dynam...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383324</comments>
            <pubDate>Tue, 25 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383324</guid>        </item>
        <item>
            <title>Soluble Î²-glucan from Grifola frondosa induces proliferation and Dectin-1/Syk signaling in resident macrophages via the GM-CSF autocrine pathway.</title>
            <link>http://www.medworm.com/index.php?rid=5383323&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22028332%26dopt%3DAbstract</link>
            <description>In conclusion, we demonstrated that MD-Fraction induces cell proliferation and cytokine production without excessive inflammation in resident macrophages, supporting its immunotherapeutic potential.
    PMID: 22028332 [PubMed - as supplied by publisher] (Source: Journal of Leukocyte Biology)</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383323</comments>
            <pubDate>Tue, 25 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383323</guid>        </item>
        <item>
            <title>Fc receptor-like 5 promotes B cell proliferation and drives the development of cells displaying switched isotypes.</title>
            <link>http://www.medworm.com/index.php?rid=5383322&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22028333%26dopt%3DAbstract</link>
            <description>Authors: Dement-Brown J, Newton CS, Ise T, Damdinsuren B, Nagata S, Tolnay M
    Abstract
    The biological roles of B cell membrane proteins in the FCRL family are enigmatic. FCRL proteins, including FCRL5, were shown to modulate early BCR signaling, although the subsequent, functional consequences of receptor engagement are poorly understood. We found that FCRL5 surface protein itself was induced temporarily upon BCR stimulation of human, naive B cells, indicating precise control over timing of FCRL5 engagement. Cross-linking of FCRL5 on cells induced to express FCRL5 enhanced B cell proliferation significantly. This enhancement required costimulation of the BCR and TLR9, two signals required for optimal proliferation of naive B cells, whereas T cell help in the form of anti-CD40 and IL...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383322</comments>
            <pubDate>Tue, 25 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383322</guid>        </item>
        <item>
            <title>The glucocorticoid dexamethasone programs human dendritic cells for enhanced phagocytosis of apoptotic neutrophils and inflammatory response.</title>
            <link>http://www.medworm.com/index.php?rid=5383321&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22028334%26dopt%3DAbstract</link>
            <description>Authors: Hodrea J, Majai G, DorÃ³ Z, Zahuczky G, Pap A, RajnavÃ¶lgyi E, FÃ©sÃ¼s L
    Abstract
    GCs are powerful anti-inflammatory compounds inhibiting inflammatory cell recruitment and production of proinflammatory cytokines. We have recently found that DCs, the key players of T cell priming and polarization, respond to allogeneic apoptotic neutrophils with proinflammatory cytokine release and Th1 cell activation. Here, we show that monocyte-derived human DCs develop their capacity to engulf apoptotic cells by up-regulating a set of apoptophagocytic genes. This gene expression pattern was reprogrammed when differentiation took place in the presence of the synthetic GC Dex, which increased the expression of phagocytosis receptors MERTK and CD14, the bridging molecule C1QA, DNASE2, and A...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383321</comments>
            <pubDate>Tue, 25 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383321</guid>        </item>
        <item>
            <title>Mobilization of hematopoietic stem and leukemia cells.</title>
            <link>http://www.medworm.com/index.php?rid=5383320&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22028335%26dopt%3DAbstract</link>
            <description>Authors: Schroeder MA, Dipersio JF
    Abstract
    HSC mobilization is an essential homeostatic process during inflammation and for the maintenance of hematopoietic progenitors. It has been exploited for the therapeutic application of HSC transplantation. Recent evidence suggests that leukemic cells share surface molecules in common with stem cells and may be mobilized under similar conditions. This effect could be used for therapeutic interventions. In this review, we will provide evidence showing that leukemia cells and stem cells traffic similarly and may share a common niche. Studies are discussed comparing and contrasting the mechanism of normal stem cells and leukemic cell mobilization through the CXCR4/CXCL12 axis and other key intermediaries.
    PMID: 22028335 [PubMed - as suppli...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383320</comments>
            <pubDate>Tue, 25 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383320</guid>        </item>
        <item>
            <title>The mouse interleukin (Il)33 gene is expressed in a cell type- and stimulus-dependent manner from two alternative promoters.</title>
            <link>http://www.medworm.com/index.php?rid=5383327&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22013230%26dopt%3DAbstract</link>
            <description>Authors: Talabot-Ayer D, Calo N, Vigne S, Lamacchia C, Gabay C, Palmer G
    Abstract
    GenBank entries for mouse Il33 reveal the existence of two transcripts, Il33a and Il33b, with different 5`UTRs but coding for the same protein. We investigated expression of these transcripts in different mouse organs and cell types in basal and inflammatory conditions. Il33a and Il33b mRNAs start with different noncoding first exons, transcribed from different promoter regions, which both contain a consensus TATA-like sequence. Constitutive Il33a mRNA expression was detected in mouse stomach, lung, spleen, and brain, whereas basal Il33b mRNA expression was observed only in the stomach. Expression of both transcripts increased after systemic LPS administration. In vitro, we observed high constitutive ...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383327</comments>
            <pubDate>Wed, 19 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383327</guid>        </item>
        <item>
            <title>Pivotal Advance: Invariant NKT cells reduce accumulation of inflammatory monocytes in the lungs and decrease immune-pathology during severe influenza A virus infection.</title>
            <link>http://www.medworm.com/index.php?rid=5383330&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22003207%26dopt%3DAbstract</link>
            <description>Authors: Kok WL, Denney L, Benam K, Cole S, Clelland C, McMichael AJ, Ho LP
    Abstract
    Little is known of how a strong immune response in the lungs is regulated to minimize tissue injury during severe influenza A virus (IAV) infection. Here, using a model of lethal, high-pathogenicity IAV infection, we first show that Ly6C(hi)Ly6G(-) inflammatory monocytes, and not neutrophils, are the main infiltrate in lungs of WT mice. Mice devoid of iNKT cells (JÎ±18(-/-) mice) have increased levels of inflammatory monocytes, which correlated with increased lung injury and mortality (but not viral load). Activation of iNKT cells correlated with reduction of MCP-1 levels and improved outcome. iNKT cells were able to selectively lyse infected, MCP-1-producing monocytes in vitro, in a CD1d-dependent...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383330</comments>
            <pubDate>Fri, 14 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383330</guid>        </item>
        <item>
            <title>Serine phosphorylation of Fc{gamma}RI cytoplasmic domain directs lipid raft localization and interaction with protein 4.1G.</title>
            <link>http://www.medworm.com/index.php?rid=5383329&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22003208%26dopt%3DAbstract</link>
            <description>Authors: Gibson AW, Li X, Wu J, Baskin JG, Raman C, Edberg JC, Kimberly RP
    Abstract
    The high-affinity IgG receptor (CD64, FcÎ³RI) has several special capacities, including the receptor-stimulated cleavage of the cell surface B cell-activating factor of the TNF superfamily (TNFSF13B). With the use of the yeast two-hybrid system, we and others have shown that FcÎ³RI interacts with protein 4.1G (EPB41L2). Our mutational analyses identified two required 4.1G-interacting regions in the FcÎ³RI CY and one FcÎ³RI-interacting site in the C-terminus of protein 4.1G. Herein, we explore mechanism(s) that may regulate the interaction between protein 4.1G and FcÎ³RI CY and influence FcÎ³RI membrane mobility and function. We show that FcÎ³RI CY interacts with protein 4.1G in vitro and that FcÎ³RI...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383329</comments>
            <pubDate>Fri, 14 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383329</guid>        </item>
        <item>
            <title>High MafB expression following burn augments monocyte commitment and inhibits DC differentiation in hemopoietic progenitors.</title>
            <link>http://www.medworm.com/index.php?rid=5383331&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21984745%26dopt%3DAbstract</link>
            <description>Authors: Howell K, Posluszny J, He LK, Szilagyi A, Halerz J, Gamelli RL, Shankar R, Muthu K
    Abstract
    We have previously shown that perturbed bone marrow progenitor development promotes hyporesponsive monocytes following experimental burn sepsis. Clinical and experimental sepsis is associated with monocyte deactivation and depletion of mDCs. Decrease in circulating DCs is reported in burn patients who develop sepsis. In our 15% TBSA scald burn model, we demonstrate a significant reduction in the circulating MHC-II(+) population and mDCs (Gr1(neg)CD11b(+)CD11c(+)) with a corresponding decrease in bone marrow MHC-II(+) cells and mDCs for up to 14 days following burn. We explored the underlying mechanism(s) that regulate bone marrow development of monocytes and DCs following burn injur...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383331</comments>
            <pubDate>Fri, 07 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383331</guid>        </item>
        <item>
            <title>p38 Mitogen-activated protein kinase signaling regulates streptococcal M1 protein-induced neutrophil activation and lung injury.</title>
            <link>http://www.medworm.com/index.php?rid=5383333&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21971519%26dopt%3DAbstract</link>
            <description>In conclusion, these findings suggest that targeting the p38 MAPK signaling pathway may open new opportunities to protect against lung injury in streptococcal infections.
    PMID: 21971519 [PubMed - as supplied by publisher] (Source: Journal of Leukocyte Biology)</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383333</comments>
            <pubDate>Tue, 04 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383333</guid>        </item>
        <item>
            <title>Enhanced Toll-like receptor (TLR) responses of TNFR-associated factor 3 (TRAF3)-deficient B lymphocytes.</title>
            <link>http://www.medworm.com/index.php?rid=5383332&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21971520%26dopt%3DAbstract</link>
            <description>Authors: Xie P, Poovassery J, Stunz LL, Smith SM, Schultz ML, Carlin LE, Bishop GA
    Abstract
    The key role of TRAF6 in TLR signaling pathways is well known. More recent evidence has implicated TRAF3 as another TRAF family member important to certain TLR responses of myeloid cells. Previous studies demonstrate that TRAF3 functions are highly context-dependent, displaying receptor and cell-type specificity. We thus examined the TLR responses of TRAF3(-/-)mouse B lymphocytes to test the hypothesis that TRAF3 plays distinct roles in such responses, depending on cell type. TRAF3(-/-) DC are known to have a defect in type 1 IFN production and here, showed diminished production of TNF and IL-10 and unaltered IL-6. In marked contrast, TRAF3(-/-) B cells made elevated amounts of TNF and IL-6 ...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383332</comments>
            <pubDate>Tue, 04 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383332</guid>        </item>
        <item>
            <title>Developmental regulation of P-glycoprotein activity within thymocytes results in increased anti-HIV protease inhibitor activity.</title>
            <link>http://www.medworm.com/index.php?rid=5284131&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21504949%26dopt%3DAbstract</link>
            <description>This study demonstrates that CXCR4-using WT viruses are more sensitive to PI in fetal thymcocytes than mature T cells with average IC(50) values for two PIs, RTV and IDV, of 1.5 nM (RTV) and 4.4 nM (IDV) in thymocytes versus 309.4 nM (RTV) and 27.3 nM (IDV) in mature T cells. P-gp activity, as measured using Rh123 efflux and quantitation of P-gp mRNA, increased with thymocyte maturation into CD4 and CD8 lineage T cells. P-gp activity is developmentally regulated in the thymus. Thymocytes developed increased levels of P-gp activity as maturation from DP to SP CD4 or CD8 T cells occurred, although CD4 T cells acquired activity more rapidly. Reduced P-gp activity in thymocytes is one mechanism for effectiveness of PI therapy in suppressing viral replication in the thymus and in reconstitution...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284131</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5284131</guid>        </item>
        <item>
            <title>Technical Advance: Soluble OX40 molecule mimics regulatory T cell modulatory activity on Fc{varepsilon}RI-dependent mast cell degranulation.</title>
            <link>http://www.medworm.com/index.php?rid=5284130&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21653238%26dopt%3DAbstract</link>
            <description>Authors: Sibilano R, Gri G, Frossi B, Tripodo C, Suzuki R, Rivera J, Macdonald AS, Pucillo CE
    Abstract
    Tregs play a central role in modulating FcÎµRI-dependent MC effector functions in the course of the allergic response. Cellular interaction depends on the constitutive expression of OX40 on Tregs and the OX40L counterpart on MCs. Study of OX40L signaling on MCs is hampered by the need of a highly purified molecule, which triggers OX40L specifically. We now report that sOX40 mimics the physiological activity of Treg interaction by binding to activated MCs. When treated with sOX40, activated MCs showed decreased degranulation and Ca(++) influx, whereas PLC-Î³2 phosphorylation remained unaffected. Once injected into experimental animals, sOX40 not only located within the endothelium ...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284130</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5284130</guid>        </item>
        <item>
            <title>Editorial: Granulopoiesis versus monopoiesis: a consequence of transcription factors dancing with the right partners.</title>
            <link>http://www.medworm.com/index.php?rid=5284127&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21965310%26dopt%3DAbstract</link>
            <description>Authors: Sakamoto KM
    PMID: 21965310 [PubMed - in process] (Source: Journal of Leukocyte Biology)</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284127</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5284127</guid>        </item>
        <item>
            <title>Editorial: Developmental regulation of P-glycoprotein and HIV therapy: spare the thymus but spoil the child?</title>
            <link>http://www.medworm.com/index.php?rid=5284126&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21965311%26dopt%3DAbstract</link>
            <description>Authors: Krogstad P, Aldrovandi G
    PMID: 21965311 [PubMed - in process] (Source: Journal of Leukocyte Biology)</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284126</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5284126</guid>        </item>
        <item>
            <title>The myosin family: unconventional roles of actin-dependent molecular motors in immune cells.</title>
            <link>http://www.medworm.com/index.php?rid=5284129&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21965174%26dopt%3DAbstract</link>
            <description>Authors: Maravillas-Montero JL, Santos-Argumedo L
    Abstract
    Myosins comprise a family of ATP-dependent motor proteins that are best known for their role in muscle contraction and their involvement in a wide range of other eukaryotic motility processes. Recent phylogenetic analysis places myosins into 35 highly diverse classes. Although these actin-based molecular motors have been characterized extensively, and much is known about their function in different cellular compartments, there is little information available about these molecules in hematopoietic cells. The available data establish that myosins expressed by immune cells are able to support general tasks, such as maintaining plasma membrane tension, moving and secreting vesicles, aiding in endo- and exocytotic processes, and...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284129</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5284129</guid>        </item>
        <item>
            <title>Estradiol impairs the Th17 immune response against Candida albicans.</title>
            <link>http://www.medworm.com/index.php?rid=5284128&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21965175%26dopt%3DAbstract</link>
            <description>We report that estradiol increases mouse susceptibility to systemic candidiasis, as in vivo and ex vivo estradiol-treated DCs were less efficient at up-regulating antigen-presenting machinery, pathogen killing, migration, IL-23 production, and triggering of the Th17 immune response. Based on these results, we propose that estradiol impairs DC function, thus explaining the increased susceptibility to infection during estrus.
    PMID: 21965175 [PubMed - as supplied by publisher] (Source: Journal of Leukocyte Biology)</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284128</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5284128</guid>        </item>
        <item>
            <title>The multiple roles of the CD8 coreceptor in T cell biology: opportunities for the selective modulation of self-reactive cytotoxic T cells.</title>
            <link>http://www.medworm.com/index.php?rid=5284135&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21954283%26dopt%3DAbstract</link>
            <description>Authors: Laugel B, Cole DK, Clement M, Wooldridge L, Price DA, Sewell AK
    Abstract
    Short peptide fragments generated by intracellular protein cleavage are presented on the surface of most nucleated cells bound to highly polymorphic MHCI molecules. These pMHCI complexes constitute an interface that allows the immune system to identify and eradicate anomalous cells, such as those that harbor infectious agents, through the activation of CTLs. Molecular recognition of pMHCI complexes is mediated primarily by clonally distributed TCRs expressed on the surface of CTLs. The coreceptor CD8 contributes to this antigen-recognition process by binding to a largely invariant region of the MHCI molecule and by promoting intracellular signaling, the effects of which serve to enhance TCR stimuli tr...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284135</comments>
            <pubDate>Tue, 27 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5284135</guid>        </item>
        <item>
            <title>Characterization of the nature of granulocytic myeloid-derived suppressor cells in tumor-bearing mice.</title>
            <link>http://www.medworm.com/index.php?rid=5284134&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21954284%26dopt%3DAbstract</link>
            <description>In this study, we have found that G-MDSCs, from tumor-bearing, and Neu, from tumor-free, mice share a common morphology and phenotype. However, in contrast to Neu, a substantial proportion of G-MDSCs expressed M-CSFR and a CD244 molecule. Neu had significantly higher phagocytic activity, expression of lysosomal proteins, and TNF-Î± than corresponding G-MDSCs, which had significantly higher activity of arginase, MPO, and ROS. In contrast to G-MDSC, neither rested nor mobilized Neu suppressed T cells. G-MDSC survived 2 days in culture in the presence of GM-CSF and within 24 h, became phenotypic and functionally similar to Neu. Tumor-associated G-MDSC shared most characteristics of splenic G-MDSC, rather then Neu. These data suggest that in cancer, despite morphological and phenotypic similar...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284134</comments>
            <pubDate>Tue, 27 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5284134</guid>        </item>
        <item>
            <title>{alpha}-Tocopherol induces hematopoietic stem/progenitor cell expansion and ERK1/2-mediated differentiation.</title>
            <link>http://www.medworm.com/index.php?rid=5284133&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21954285%26dopt%3DAbstract</link>
            <description>Authors: Nogueira-Pedro A, Barbosa CM, Segreto HR, Lungato L, D'Almeida V, Moraes AA, Miranda A, Paredes-Gamero EJ, Ferreira AT
    Abstract
    Tocopherols promote or inhibit growth in different cell types. In the hematopoietic system, the radioprotective property of tocopherols is thought to act through the expansion of primitive hematopoietic cells, however, the mechanisms activated by tocopherols and which HPs are affected remain poorly understood. To better address these questions, mice were treated with Î±-tocopherol, and its effects were investigated in the BM microenvironment. Î±-Tocopherol induced increased proliferation in HSC/HP cells, leading to BM hyperplasia. In addition, differentiation to the granulocytic/monocytic lineage was enhanced by Î±-tocopherol treatment. Î±-Tocophe...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284133</comments>
            <pubDate>Tue, 27 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5284133</guid>        </item>
        <item>
            <title>Stable accumulation of p67phox at the phagosomal membrane and ROS production within the phagosome.</title>
            <link>http://www.medworm.com/index.php?rid=5284132&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21954286%26dopt%3DAbstract</link>
            <description>Authors: Tlili A, Erard M, Faure MC, Baudin X, Piolot T, DuprÃ©-Crochet S, NÃ¼ÃŸe O
    Abstract
    Production of ROS by the leukocyte NADPH oxidase is essential for the destruction of pathogenic bacteria inside phagosomes. The enzyme is a complex of cytosolic and membranous subunits that need to assemble upon activation. Biochemical data suggest that the complex is renewed continuously during activity. Furthermore, it is generally assumed that complex assembly and activity occur in parallel. However, information about the oxidase assembly in individual phagosomes in live cells is scarce. We studied the dynamic behavior of the crucial cytosolic NADPH oxidase component p67(phox) during phagocytosis by videomicroscopy. p67(phox) is involved in the regulation of electron flow from NADPH to o...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284132</comments>
            <pubDate>Tue, 27 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5284132</guid>        </item>
        <item>
            <title>Human CD16+ and CD16- monocyte subsets display unique effector properties in inflammatory conditions in vivo.</title>
            <link>http://www.medworm.com/index.php?rid=5249657&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21937707%26dopt%3DAbstract</link>
            <description>Authors: Aguilar-Ruiz SR, Torres-Aguilar H, GonzÃ¡lez-DomÃ­nguez E, NarvÃ¡ez J, GonzÃ¡lez-PÃ©rez G, Vargas-Ayala G, Meraz-RÃ­os MA, GarcÃ­a-Zepeda EA, SÃ¡nchez-Torres C
    Abstract
    Two major subsets of human Mo are identified based on CD14 and CD16 expression: the classical CD16(-) Mo and the minor CD14(+)CD16(+) Mo. In vitro studies suggested distinct function and differentiation potential for each cell population. However, the in vivo relevance of these findings remains unclear. To evaluate the development and function of human Mo in an in vivo model, we transferred both Mo subpopulations into the peritoneum of immunocompromised mice in homeostatic or inflammatory conditions. Inflammation was induced with soluble LPS or particulate zymosan. CD16(+) were more phagocytic and produced ...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5249657</comments>
            <pubDate>Wed, 21 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5249657</guid>        </item>
        <item>
            <title>Higher proportions of circulating FOXP3+ and CTLA-4+ regulatory T cells are associated with lower fractions of memory CD4+ T cells in infants.</title>
            <link>http://www.medworm.com/index.php?rid=5249663&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21934066%26dopt%3DAbstract</link>
            <description>In conclusion, FOXP3(+) or CTLA-4(+) T(regs) may modulate CD4(+) T cell activation and homing receptor expression in children.
    PMID: 21934066 [PubMed - as supplied by publisher] (Source: Journal of Leukocyte Biology)</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5249663</comments>
            <pubDate>Tue, 20 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5249663</guid>        </item>
        <item>
            <title>C-reactive protein-derived peptide 201-206 inhibits neutrophil adhesion to endothelial cells and platelets through CD32.</title>
            <link>http://www.medworm.com/index.php?rid=5249662&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21934067%26dopt%3DAbstract</link>
            <description>Authors: El Kebir D, Zhang Y, Potempa LA, Wu Y, Fournier A, Filep JG
    Abstract
    The role of CRP as a regulator of inflammation is not fully understood. Structural rearrangement in CRP results in expression of potent proinflammatory actions. Proteolysis of CRP yields the C-terminal peptide Lys(201)-Pro-Gln-Leu-Trp-Pro(206). Here, we investigated the impact of this peptide on neutrophil interactions with endothelial cells and platelets, critical inflammatory events triggering acute coronary artery disease. CRP peptide 201-206 induced L-selectin shedding from human neutrophils and inhibited L-selectin-mediated neutrophil adhesion to TNF-Î±-activated HCAECs under nonstatic conditions. CRP peptide 201-206 also attenuated shear-induced up-regulation of platelet P-selectin expression, plate...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5249662</comments>
            <pubDate>Tue, 20 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5249662</guid>        </item>
        <item>
            <title>Myeloid-derived suppressor cells help protective immunity to Leishmania major infection despite suppressed T cell responses.</title>
            <link>http://www.medworm.com/index.php?rid=5249661&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21934068%26dopt%3DAbstract</link>
            <description>Authors: Pereira WF, Ribeiro-Gomes FL, Guillermo LV, Vellozo NS, MontalvÃ£o F, Dosreis GA, Lopes MF
    Abstract
    Th1/Th2 cytokines play a key role in immune responses to Leishmania major by controlling macrophage activation for NO production and parasite killing. MDSCs, including myeloid precursors and immature monocytes, produce NO and suppress T cell responses in tumor immunity. We hypothesized that NO-producing MDSCs could help immunity to L. major infection. Gr1(hi)(Ly6C(hi)) CD11b(hi) MDSCs elicited by L. major infection suppressed polyclonal and antigen-specific T cell proliferation. Moreover, L. major-induced MDSCs killed intracellular parasites in a NO-dependent manner and reduced parasite burden in vivo. By contrast, treatment with ATRA, which induces MDSCs to differentiate in...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5249661</comments>
            <pubDate>Tue, 20 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5249661</guid>        </item>
        <item>
            <title>Investigation of the differential potentials of TLR agonists to elicit uveitis in mice.</title>
            <link>http://www.medworm.com/index.php?rid=5249660&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21934069%26dopt%3DAbstract</link>
            <description>Authors: Allensworth JJ, Planck SR, Rosenbaum JT, Rosenzweig HL
    Abstract
    TLRs are critical for host defense and innate immunity. Emerging evidence also supports a role for TLRs in many chronic inflammatory diseases, including inflammatory eye disease, known as uveitis. The activation of TLR4 by endotoxin induces a standard model of murine uveitis. How activation of additional TLRs influences the onset and/or severity of anterior uveitis has not been examined. We sought to elucidate the potential of TLRs (TLR1/2, TLR2/6, TLR3, TLR4, TLR5, TLR7/8, and TLR9) to trigger uveitis in mice. Directly stimulated iris/ciliary body explants demonstrated a marked increase in production of inflammatory cytokines TNF-Î±, IL-6, IP-10/CXCL10, MCP-1, and KC with relatively little production of IFN-Î...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5249660</comments>
            <pubDate>Tue, 20 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5249660</guid>        </item>
        <item>
            <title>Induction of endotoxin tolerance in vivo inhibits activation of IRAK4 and increases negative regulators IRAK-M, SHIP-1, and A20.</title>
            <link>http://www.medworm.com/index.php?rid=5249659&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21934070%26dopt%3DAbstract</link>
            <description>Authors: Xiong Y, Medvedev AE
    Abstract
    TLRs mediate host defense against microbial pathogens by eliciting production of inflammatory mediators and activating expression of MHC, adhesion, and costimulatory molecules. Endotoxin tolerance limits excessive TLR-driven inflammation during sepsis and reprograms macrophage responses to LPS, decreasing expression of proinflammatory cytokines without inhibiting anti-inflammatory and antimicrobial mediators. Molecular mechanisms of reprogramming of TLR4 signaling upon in vivo induction of endotoxin tolerance are incompletely understood. We used an in vivo model of endotoxin tolerance, whereby C57BL/6 mice were i.p.-inoculated with LPS or PBS, followed by in vitro challenge of peritoneal or splenic macrophages with LPS to examine activation of...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5249659</comments>
            <pubDate>Tue, 20 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5249659</guid>        </item>
        <item>
            <title>Facilitated antigen uptake and timed exposure to TLR ligands dictate the antigen-presenting potential of plasmacytoid DCs.</title>
            <link>http://www.medworm.com/index.php?rid=5249658&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21934071%26dopt%3DAbstract</link>
            <description>Authors: Kool M, Geurtsvankessel C, Muskens F, Branco Madeira F, van Nimwegen M, Kuipers H, Thielemans K, Hoogsteden HC, Hammad H, Lambrecht BN
    Abstract
    Subsets of antigen-presenting cDCs have a differential capacity to present exogenous and endogenous protein antigens to CD4(+) and/or CD8(+) T lymphocytes, depending on expression of antigen-uptake receptors, processing machinery, and microbial instruction. pDCs are also capable of antigen presentation, but the conditions under which they do this have not been systematically addressed. Highly purified cDCs and pDCs were exposed to exogenous, soluble OVA peptide or whole protein. Alternatively, they were made to express cytoplasmic or endosomal OVA by retroviral transduction or by infection with influenza virus containing OVA epitop...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5249658</comments>
            <pubDate>Tue, 20 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5249658</guid>        </item>
        <item>
            <title>Tregs and infections: on the potential value of modifying their function.</title>
            <link>http://www.medworm.com/index.php?rid=5221590&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21914856%26dopt%3DAbstract</link>
            <description>Authors: Sehrawat S, Rouse BT
    Abstract
    CD4(+) T cells, which express a master transcription factor, Foxp3, have been recognized as bona fide Tregs. These cells are essential to maintain immune homeostasis in healthy as well as infected mice and humans. Extensive investigations in the last decade have provided ways to manipulate the Foxp3(+) Treg response therapeutically so the role of such cells in microbe-induced inflammatory reactions can be evaluated. This review focuses on our current understanding of the mechanisms required for the generation and sustenance of Tregs in vivo and the potential value of modulating Tregs to control microbe-induced immunopathological responses.
    PMID: 21914856 [PubMed - as supplied by publisher] (Source: Journal of Leukocyte Biology)</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221590</comments>
            <pubDate>Tue, 13 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5221590</guid>        </item>
        <item>
            <title>Editorial: Ilya Metchnikoff, the phagocytic theory, and how things often work in science.</title>
            <link>http://www.medworm.com/index.php?rid=5195574&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21880643%26dopt%3DAbstract</link>
            <description>Authors: Silverstein AM
    PMID: 21880643 [PubMed - in process] (Source: Journal of Leukocyte Biology)</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5195574</comments>
            <pubDate>Wed, 31 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5195574</guid>        </item>
        <item>
            <title>Editorial: The double life of M-ficolin: what functions when circulating in serum and tethered to leukocyte surfaces?</title>
            <link>http://www.medworm.com/index.php?rid=5195573&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21880644%26dopt%3DAbstract</link>
            <description>Authors: Thielens NM
    PMID: 21880644 [PubMed - in process] (Source: Journal of Leukocyte Biology)</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5195573</comments>
            <pubDate>Wed, 31 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5195573</guid>        </item>
        <item>
            <title>Modulating impact of human chorionic gonadotropin hormone on the maturation and function of hematopoietic cells.</title>
            <link>http://www.medworm.com/index.php?rid=5180379&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21878542%26dopt%3DAbstract</link>
            <description>This study in MNCs of women who received hCG as preconditioning prior to IVF demonstrates that hCG increases anti-inflammatory IL-27 expression and reduces inflammatory IL-17 expression. In addition, we found increased IL-10 levels and elevated numbers of Tregs in peripheral blood of women after hCG application. Rejection of allogeneic skin grafts was delayed in female mice receiving hCG. We conclude that hCG may be useful for the induction of immune tolerance in solid organ transplantation.
    PMID: 21878542 [PubMed - as supplied by publisher] (Source: Journal of Leukocyte Biology)</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5180379</comments>
            <pubDate>Mon, 29 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5180379</guid>        </item>
        <item>
            <title>Defective eosinophil hematopoiesis ex vivo in inbred Rocky Mountain White (IRW) mice.</title>
            <link>http://www.medworm.com/index.php?rid=5180378&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21878543%26dopt%3DAbstract</link>
            <description>Authors: Dyer KD, Garcia-Crespo KE, Percopo CM, Bowen AB, Ito T, Peterson KE, Gilfillan AM, Rosenberg HF
    Abstract
    We examine the proliferation and differentiation of bone marrow (BM) progenitors from inbred Rocky Mountain White (IRW) mice, a strain used primarily for retrovirus infection studies. In contrast to findings with BALB/c and C57BL/6 strains, IRW BM cells cannot proliferate or generate pure eosinophil cultures ex vivo in response to a defined cytokine regimen. Analysis of IRW BM at baseline was unremarkable, including 0.08 Â± 0.03% Lin(-)Sca-1(+)c-kit(+ )(LSK) hematopoietic stem cells and 5.2 Â± 0.3% eosinophils; the percentage of eosinophil progenitors (EoPs; Lin(-)Sca-1(-) c-kit(+)CD34(+)IL-5RÎ±(+)) was similar in all three mouse strains. Transcripts encoding GM-CSFRÎ± ...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5180378</comments>
            <pubDate>Mon, 29 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5180378</guid>        </item>
        <item>
            <title>Macrophage phagocytosis: effects of environmental pollutants, alcohol, cigarette smoke, and other external factors.</title>
            <link>http://www.medworm.com/index.php?rid=5180377&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21878544%26dopt%3DAbstract</link>
            <description>Authors: Karavitis J, Kovacs EJ
    Abstract
    The ability of a pathogen to evade host immunity successfully, in contrast to the host's capacity to defend itself against a foreign invader, is a complex struggle, in which eradication of infection is dictated by a robust immunologic response. Often, there are external factors that can alter the outcome by tipping the scale to benefit pathogen establishment rather than resolution by the host's defense system. These external sources, such a cigarettes, alcohol, or environmental pollutants, can negatively influence the effectiveness of the immune system's response to a pathogen. The observed suppression of immune function can be attributed to dysregulated cytokine and chemokine production, the loss of migratory potential, or the inability to ...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5180377</comments>
            <pubDate>Mon, 29 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5180377</guid>        </item>
        <item>
            <title>Inhibitory effect of semaphorin-3A, a known axon guidance molecule, in the human thymocyte migration induced by CXCL12.</title>
            <link>http://www.medworm.com/index.php?rid=5180376&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21878545%26dopt%3DAbstract</link>
            <description>Authors: Garcia F, Lepelletier Y, Smaniotto S, Hadj-Slimane R, Dardenne M, Hermine O, Savino W
    Abstract
    Intrathymic T cell differentiation takes place within the thymic lobules and depends on interactions between developing thymocytes and cells of the thymic microenvironment. Along with differentiation, thymocytes migrate in an oriented progression, which is tightly regulated by a number of interactions, including one mediated by the chemokine CXCL12. It has been shown recently that SEMA-3A, a soluble member of the semaphorin family, is also involved in this human thymocyte migration and can have a chemorepulsive and de-adhesive role. Herein, we study the role of SEMA-3A on the CXCL12-driven migration of human thymocytes. We have shown that SEMA-3A is able to inhibit the chemotaxis...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5180376</comments>
            <pubDate>Mon, 29 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5180376</guid>        </item>
        <item>
            <title>Aquaporin 9 phosphorylation mediates membrane localization and neutrophil polarization.</title>
            <link>http://www.medworm.com/index.php?rid=5180383&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21873454%26dopt%3DAbstract</link>
            <description>Authors: Karlsson T, Glogauer M, Ellen RP, Loitto VM, Magnusson KE, MagalhÃ£es MA
    Abstract
    Neutrophils are of prime importance in the host innate defense against invading microorganisms by using two primary mechanisms-locomotion toward and phagocytosis of the prey. Recent research points to pivotal roles for water channels known as AQPs in cell motility. Here, we focused on the role of AQP9 in chemoattractant-induced polarization and migration of primary mouse neutrophils and neutrophil-like HL60 cells. We found that AQP9 is phosphorylated downstream of fMLFR or PMA stimulation in primary human neutrophils. The dynamics of AQP9 were assessed using GFP-tagged AQP9 constructs and other fluorescent markers through various live-cell imaging techniques. Expression of WT or the phosphomi...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5180383</comments>
            <pubDate>Thu, 25 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5180383</guid>        </item>
        <item>
            <title>Deletion of cannabinoid receptors 1 and 2 exacerbates APC function to increase inflammation and cellular immunity during influenza infection.</title>
            <link>http://www.medworm.com/index.php?rid=5180382&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21873455%26dopt%3DAbstract</link>
            <description>In this study, we demonstrate that APC function is enhanced specifically in the absence of CB(1) and CB(2) signaling, resulting in an exacerbated immune response phenotype. After influenza infection, CB(1)(-/-)CB(2)(-/-) mice showed more pronounced pulmonary damage, increased inflammatory cell infiltrate, inflammation, and a greater cellular immune responses compared with WT mice, as evidenced by transcriptome analysis, more robust T cell activation, and effector cell cytokine production. After direct activation in vitro, there were no differences in the percentages of cytokine-producing CD4(+) T cells between CB(1)(-/-)CB(2)(-/-) and WT mice. However, untreated CB(1)(-/-)CB(2)(-/-) mice routinely had fewer naÃ¯ve T cells compared with WT, suggesting dysregulation of APC immune homeostasis...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5180382</comments>
            <pubDate>Thu, 25 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5180382</guid>        </item>
        <item>
            <title>Differentiation of CD8+ T cells into effector cells is enhanced by physiological range hyperthermia.</title>
            <link>http://www.medworm.com/index.php?rid=5180381&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21873456%26dopt%3DAbstract</link>
            <description>In this study, we asked whether exposure to different physiologically relevant temperatures (33Â°C, 37Â°C, and 39.5Â°C) could affect subsequent antigen-specific, activation-related events of naive CD8(+) T cells. We observed that temporary exposure of CD62L(hi)CD44(lo) Pmel-1 CD8(+) cells to 39.5Â°C prior to their antigen-dependent activation with gp100(25-33) peptide-pulsed C57BL/6 splenocytes resulted in a greater percentage of cells, which eventually differentiated into CD62L(lo)CD44(hi) effector cells compared with cells incubated at 33Â°C and 37Â°C. However, the proliferation rate of naive CD8(+) T cells was not affected by mild heating. While exploring these effects further, we observed that mild heating of CD8(+) T cells resulted in the reversible clustering of GM1(+) CD-microdomain...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5180381</comments>
            <pubDate>Thu, 25 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5180381</guid>        </item>
        <item>
            <title>Maternal KIR and fetal HLA-C: a fine balance.</title>
            <link>http://www.medworm.com/index.php?rid=5180380&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21873457%26dopt%3DAbstract</link>
            <description>Authors: Chazara O, Xiong S, Moffett A
    Abstract
    NK cell effector function is regulated by a range of activating and inhibitory receptors, and many of their known ligands are MHC class I molecules. Human NK receptors encoded by the Killer immunoglobulin-like receptor (KIR) gene family recognize polymorphic HLA-C as well as some HLA-A and HLA-B molecules. KIRs are expressed by uterine NK (uNK) cells, which are distinctive NK cells directly in contact with the invading fetal placental cells that transform the uterine arteries during the first trimester. Trophoblast cells express both maternal and paternal HLA-C allotypes and can therefore potentially interact with KIRs expressed by uNK. Therefore, allorecognition of paternal HLA-C by maternal KIR might influence trophoblast invasion a...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5180380</comments>
            <pubDate>Thu, 25 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5180380</guid>        </item>
        <item>
            <title>Tim-3 regulates pro- and anti-inflammatory cytokine expression in human CD14+ monocytes.</title>
            <link>http://www.medworm.com/index.php?rid=5142774&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21844165%26dopt%3DAbstract</link>
            <description>Authors: Zhang Y, Ma CJ, Wang JM, Ji XJ, Wu XY, Moorman JP, Yao ZQ
    Abstract
    Tim-3 and PD-1 are powerful immunoinhibitory molecules involved in immune tolerance, autoimmune responses, and antitumor or antiviral immune evasion. A current model for Tim-3 regulation during immune responses suggests a divergent function, such that Tim-3 acts synergistically with TLR signaling pathways in innate immune cells to promote inflammation, yet the same molecule terminates Th1 immunity in adaptive immune cells. To better understand how Tim-3 might be functioning in innate immune responses, we examined the kinetics of Tim-3 expression in human CD14(+) M/M(Ð¤) in relation to expression of IL-12, a key cytokine in the transition of innate to adaptive immunity. Here, we show that Tim-3 is constituti...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5142774</comments>
            <pubDate>Sun, 14 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5142774</guid>        </item>
        <item>
            <title>TLR7/9 versus TLR3/MDA5 signaling during virus infections and diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=5142773&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21844166%26dopt%3DAbstract</link>
            <description>Authors: Swiecki M, McCartney SA, Wang Y, Colonna M
    Abstract
    IFN-I are pleiotropic cytokines that impact innate and adaptive immune responses. In this article, we discuss TLR7/9 versus TLR3/MDA5 signaling in antiviral responses and diabetes. pDCs are thought to have a critical role in antiviral defense because of their ability to rapidly secrete large amounts of IFN-I through TLR7/9 signaling. A recent study demonstrates that although pDCs are a source of IFN-I in vivo, their overall contribution to viral containment is limited and time-dependent, such that additional cellular sources of IFN-I are required to fully control viral infections. dsRNA sensors, such as TLR3 and MDA5, provide another important trigger for antiviral IFN-I responses, which can be exploited to enhance immune...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5142773</comments>
            <pubDate>Sun, 14 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5142773</guid>        </item>
        <item>
            <title>Molecular analysis of the membrane insertion domain of proteinase 3, the Wegener's autoantigen, in RBL cells: implication for its pathogenic activity.</title>
            <link>http://www.medworm.com/index.php?rid=5111887&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21821719%26dopt%3DAbstract</link>
            <description>This study performed in RBL cells identifies the structural motifs of PR3 membrane anchorage and examines its impact on PR3 proinflammatory and proliferative functions. With the use of MD simulations and mutagenesis, we demonstrate that the mutations of four hydrophobic (F180, F181, L228, F229) or four basic (R193, R194, K195, R227) amino acids abrogated PR3 membrane anchorage. The hydrophobic patch-deficient PR3 mutant (PR34H4A) was still able to cleave the synthetic substrate Boc-Ala-Pro-Val in cell lysates. However, in contrast to WT PR3, PR34H4A was not expressed at the plasma membrane after degranulation and failed to cleave extracellular fibronectin, was not externalized after apoptosis and did not impair macrophage phagocytosis of apoptotic cells, did not promote myeloid cell prolif...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111887</comments>
            <pubDate>Thu, 04 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111887</guid>        </item>
        <item>
            <title>A cell-intrinsic role for CaMKK2 in granulocyte lineage commitment and differentiation.</title>
            <link>http://www.medworm.com/index.php?rid=5111892&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21816924%26dopt%3DAbstract</link>
            <description>Authors: Teng EC, Racioppi L, Means AR
    Granulocytes serve a critical function in host organisms by recognizing and destroying invading microbes, as well as propagating and maintaining inflammation at sites of infection. However, the molecular pathways underpinning the development of granulocytes are poorly understood. Here, we identify a role for CaMKK2 in the restriction of granulocytic fate commitment and differentiation of myeloid progenitor cells. Following BMT, engraftment by Camkk2(-/-) donor cells resulted in the increased production of mature granulocytes in the BM and peripheral blood. Similarly, Camkk2(-/-) mice possessed elevated numbers of CMP cells and exhibited an accelerated granulopoietic phenotype in the BM. Camkk2(-/-) myeloid progenitors expressed increased levels of...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111892</comments>
            <pubDate>Wed, 03 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111892</guid>        </item>
        <item>
            <title>Role of neutrophils in the activation of trypsinogen in severe acute pancreatitis.</title>
            <link>http://www.medworm.com/index.php?rid=5111899&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21810937%26dopt%3DAbstract</link>
            <description>Authors: Abdulla A, Awla D, Thorlacius H, RegnÃ©r S
    The relationship between inflammation and proteolytic activation in pancreatitis is an unresolved issue in pancreatology. The purpose of this study was to define the influence of neutrophils on trypsinogen activation in severe AP. Pancreatitis was induced by infusion of taurocholate into the pancreatic duct in C57BL/6 mice. For neutrophil depletion, an anti-Gr-1 antibody was administered before pancreatitis induction. Administration of the anti-Gr-1 antibody reduced circulating neutrophils by 97%. Pancreatic TAP and serum amylase levels increased 2 h and 24 h after induction of pancreatitis. Neutrophil depletion reduced pancreatic TAP and serum amylase levels at 24 h but not at 2 h after pancreatitis induction. Pancreatic MPO and infi...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111899</comments>
            <pubDate>Mon, 01 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111899</guid>        </item>
        <item>
            <title>Lung dendritic cells at the innate-adaptive immune interface.</title>
            <link>http://www.medworm.com/index.php?rid=5111943&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21807741%26dopt%3DAbstract</link>
            <description>Authors: Condon TV, Sawyer RT, Fenton MJ, Riches DW
    This review updates the basic biology of lung DCs and their functions. Lung DCs have taken center stage as cellular therapeutic targets in new vaccine strategies for the treatment of diverse human disorders, including asthma, allergic lung inflammation, lung cancer, and infectious lung disease. The anatomical distribution of lung DCs, as well as the division of labor between their subsets, aids their ability to recognize and endocytose foreign substances and to process antigens. DCs can induce tolerance in or activate naÃ¯ve T cells, making lung DCs well-suited to their role as lung sentinels. Lung DCs serve as a functional signaling/sensing unit to maintain lung homeostasis and orchestrate host responses to benign and harmful foreign...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111943</comments>
            <pubDate>Sun, 31 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111943</guid>        </item>
        <item>
            <title>N-Acylhomoserine lactones are potent neutrophil chemoattractants that act via calcium mobilization and actin remodeling.</title>
            <link>http://www.medworm.com/index.php?rid=5111938&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21807742%26dopt%3DAbstract</link>
            <description>Authors: Karlsson T, Musse F, Magnusson KE, VikstrÃ¶m E
    In gram-negative bacteria, cell-cell communication based on HSL QS molecules is known to coordinate the production of virulence factors and biofilms. These bacterial signals can also modulate human immune cell behavior. Using a Transwell migration assay, we found that human primary neutrophils are strongly stimulated by 3O-C(12)-HSL and -C(10)-HSL but not C(4)-HSL in a concentration-dependent manner. Moreover, 3O-C(12)-HSL and -C(10)-HSL activate PLCÎ³1 but not -Î³2, mobilize intracellular calcium, and up-regulate IP(3)R. These changes were paralleled by F-actin accumulation, primarily in the leading edge of neutrophils, as evidenced by phalloidin staining and confocal microscopy. F- and G-actin isolation and quantification by imm...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111938</comments>
            <pubDate>Sun, 31 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111938</guid>        </item>
        <item>
            <title>Immunomodulatory and immunotoxic effects of bilirubin: molecular mechanisms.</title>
            <link>http://www.medworm.com/index.php?rid=5111932&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21807743%26dopt%3DAbstract</link>
            <description>Authors: Khan NM, Poduval TB
    The immunomodulatory and immunotoxic effects of purified UCB have not been evaluated previously at clinically relevant UCB concentrations and UCB:BSA ratios. To delineate the molecular mechanism of UCB-induced immunomodulation, immune cells were exposed to clinically relevant concentrations of UCB. It inhibited LPS-induced B cell proliferation and cytokine production from splenic macrophages. UCB (â‰¥25 Î¼M) was toxic to unfractionated splenocytes, splenic T cells, B cells, macrophages, LPS-stimulated CD19(+) B cells, human PBMCs, and RBCs. Purified UCB also was found to be toxic to splenocytes and human PBMCs. UCB induced necrosis and apoptosis in splenocytes. UCB activated the extrinsic and intrinsic pathways of apoptosis, as reflected by the markers, suc...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111932</comments>
            <pubDate>Sun, 31 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111932</guid>        </item>
        <item>
            <title>IL-8-mediated angiogenic responses of endothelial cells to lipid antigen activation of iNKT cells depend on EGFR transactivation.</title>
            <link>http://www.medworm.com/index.php?rid=5111926&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21807744%26dopt%3DAbstract</link>
            <description>This study investigated the participating effector mechanisms. In ECs, CM, derived from antigen-stimulated human iNKT cells (CM+), induced up-regulation of IL-8R CXCR2 and the phosphorylation of EGFR and of multiple intracellular signaling effectors, including FAK, Src, Erk, Jnk, p38-MAPK, and STAT1 and -3. We found that a cascade of events, which were IL-8-dependent and involved EGFR activation, was responsible for signaling through FAK and Src kinases and necessary for acquisition of angiogenic morphology, migration in a two-dimensional wound assay, and sprout outgrowth in a three-dimensional model of angiogenesis in vitro. The data support that IL-8-dependent activation of angiogenic behavior in ECs, in response to activated iNKT, involves CXCR2, transactivation of EGFR, and subsequent ...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111926</comments>
            <pubDate>Sun, 31 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111926</guid>        </item>
        <item>
            <title>Activated factor XI inhibits chemotaxis of polymorphonuclear leukocytes.</title>
            <link>http://www.medworm.com/index.php?rid=5111920&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21807745%26dopt%3DAbstract</link>
            <description>In this study, we characterized the functional consequences of FXIa binding to PMN leukocytes. FXIa reduced PMN leukocyte chemotaxis triggered by the chemokine, IL-8, or the bacterial-derived peptide, fMLP, perhaps as a result of the loss of directed migration. In summary, our data suggest that FXIa modulates the inflammatory response of PMN leukocytes by altering migration. These studies highlight the interplay between inflammation and coagulation and suggest that FXIa may play a role in innate immunity.
    PMID: 21807745 [PubMed - as supplied by publisher] (Source: Journal of Leukocyte Biology)</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111920</comments>
            <pubDate>Sun, 31 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111920</guid>        </item>
        <item>
            <title>Editorial: Scrambling for a response to G-CSF.</title>
            <link>http://www.medworm.com/index.php?rid=5111912&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21807746%26dopt%3DAbstract</link>
            <description>Authors: Broxmeyer HE, Touw IP
    
    PMID: 21807746 [PubMed - in process] (Source: Journal of Leukocyte Biology)</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111912</comments>
            <pubDate>Sun, 31 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111912</guid>        </item>
        <item>
            <title>Editorial: CD38 and retinoids: a step toward a cure.</title>
            <link>http://www.medworm.com/index.php?rid=5111905&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21807747%26dopt%3DAbstract</link>
            <description>Authors: Malavasi F
    
    PMID: 21807747 [PubMed - in process] (Source: Journal of Leukocyte Biology)</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111905</comments>
            <pubDate>Sun, 31 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111905</guid>        </item>
        <item>
            <title>TLR2-dependent modulation of dendritic cells by LT-IIa-B5, a novel mucosal adjuvant derived from a type II heat-labile enterotoxin.</title>
            <link>http://www.medworm.com/index.php?rid=5111953&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21791597%26dopt%3DAbstract</link>
            <description>Authors: Lee CH, Masso-Welch P, Hajishengallis G, Connell TD
    A host of human pathogens invades the body at mucosal surfaces. Yet, strong, protective mucosal immune responses directed against those pathogens routinely cannot be induced without the use of adjuvants. Although the strongest mucosal adjuvants are members of the family of HLTs, the inherent toxicities of HLT holotoxins preclude their clinical use. Herein, it is shown that LT-IIa-B(5 )enhances mucosal immune responses by modulating activities of DCs. i.n. immunization of mice with OVA in the presence of LT-IIa-B(5) recruited DCs to the NALT and significantly increased uptake of OVA by those DCs. Furthermore, LT-IIa-B(5) increased expression of CCR7 by DCs, which mediated enhanced migration of the cells from the NALT to the dr...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111953</comments>
            <pubDate>Mon, 25 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111953</guid>        </item>
        <item>
            <title>Protein disulfide isomerase redox-dependent association with p47phox: evidence for an organizer role in leukocyte NADPH oxidase activation.</title>
            <link>http://www.medworm.com/index.php?rid=5111950&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21791598%26dopt%3DAbstract</link>
            <description>Authors: Paes AM, VerÃ­ssimo-Filho S, GuimarÃ£es LL, Silva AC, Takiuti JT, Santos CX, Janiszewski M, Laurindo FR, Lopes LR
    Mechanisms of leukocyte NADPH oxidase regulation remain actively investigated. We showed previously that vascular and macrophage oxidase complexes are regulated by the associated redox chaperone PDI. Here, we investigated the occurrence and possible underlying mechanisms of PDI-mediated regulation of neutrophil NADPH oxidase. In a semirecombinant cell-free system, PDI inhibitors scrRNase (100 Î¼g/mL) or bacitracin (1 mM) near totally suppressed superoxide generation. Exogenously incubated, PDIoxi increased (by âˆ¼40%), whereas PDIred diminished (by âˆ¼60%) superoxide generation. No change occurred after incubation with PDI serine, mutated in all four redox cysteine...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111950</comments>
            <pubDate>Mon, 25 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111950</guid>        </item>
        <item>
            <title>Role of alloreactive KIR2DS1+ NK cells in haploidentical hematopoietic stem cell transplantation.</title>
            <link>http://www.medworm.com/index.php?rid=5111947&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21791599%26dopt%3DAbstract</link>
            <description>Authors: Marcenaro E, Carlomagno S, Pesce S, Della Chiesa M, Moretta A, Sivori S
    In allo-HSCT, donor-derived, &quot;alloreactive&quot; NK cells have been shown to play a crucial role in the treatment of acute leukemia, contributing to eradication of leukemic blasts (GvL effect) and to clearance of residual recipient DCs and T lymphocytes (thus, preventing GvHD and graft rejection, respectively). Such alloreactive NK cells do not express CD94/NKG2A but express inhibitory KIRs, specific for HLA class I allotypes, present in the donor but lacking in the recipient. This review is focused on the role of the activating KIR2DS1 receptor (specific for the C2-epitope of HLA-C) in haplo-HSCT. Recent data indicate that KIR2DS1 expression in HSC donors may represent a remarkable advantage in alloreactive NK...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111947</comments>
            <pubDate>Mon, 25 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111947</guid>        </item>
        <item>
            <title>Dendritic cells in bacteria handling in the gut.</title>
            <link>http://www.medworm.com/index.php?rid=5111959&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21771898%26dopt%3DAbstract</link>
            <description>Authors: Rescigno M
    DCs in the gut have specialized functions and are involved in maintaining intestinal homeostasis via tolerizing the microbiota and inducing immunity to pathogenic bacteria. Here, we summarize the characteristics of two major subtypes of phagocytes in the gut (CX3CR1(+) and CD103(+)) and pDCs and analyze their possible involvement in bacterial handling.
    PMID: 21771898 [PubMed - as supplied by publisher] (Source: Journal of Leukocyte Biology)</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111959</comments>
            <pubDate>Mon, 18 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111959</guid>        </item>
        <item>
            <title>Metabolism, LXR/LXR ligands, and tumor immune escape.</title>
            <link>http://www.medworm.com/index.php?rid=5111957&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21771899%26dopt%3DAbstract</link>
            <description>Authors: Russo V
    The mechanisms of tumor immune evasion have gained increasing interest among the tumor immunologists, because of their ability to suppress spontaneous and immunotherapy-elicited antitumor responses. Recent studies clearly show that the deletion of cells/molecules involved in tumor evasion is capable of restoring antitumor immune responses, ultimately leading to tumor rejection in mouse tumor models. These studies further support and strengthen the idea to target not only the cancer cell-intrinsic defects but also those affecting cells of the microenvironment, such as immune cells. The alterations of cancer cell metabolism are also emerging as important regulators of immune cell function, with particular emphasis on immune-escape mechanisms. Indeed, intermediate or fina...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111957</comments>
            <pubDate>Mon, 18 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111957</guid>        </item>
        <item>
            <title>Inhibition of fms-like tyrosine kinase 3 alleviates experimental arthritis by reducing formation of dendritic cells and antigen presentation.</title>
            <link>http://www.medworm.com/index.php?rid=5111955&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21771900%26dopt%3DAbstract</link>
            <description>Authors: Dehlin M, Andersson S, Erlandsson M, Brisslert M, Bokarewa M
    TKs are intracellular signaling molecules essential for cell homeostasis. Inhibition of TKs is used in treatment of malignancies and diabetes mellitus. The present study evaluated the role of Flt3 in antigen-induced arthritis. Mice were immunized with mBSA, and arthritis was induced by an i.a. injection of mBSA. Treatment with the Flt3 inhibitor sunitinib was started together with mBSA immunization or together with the induction of arthritis. The mBSA-injected joints were evaluated morphologically for signs of synovitis and bone/cartilage destruction. Markers of bone metabolism and antibody responses were measured by ELISA. Maturation of DCs in the bone marrow and spleen was evaluated by flow cytometry. Sunitinib tre...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111955</comments>
            <pubDate>Mon, 18 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111955</guid>        </item>
        <item>
            <title>Role of TLR signaling in Francisella tularensis-LPS-induced, antibody-mediated protection against Francisella tularensis challenge.</title>
            <link>http://www.medworm.com/index.php?rid=5111964&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21750122%26dopt%3DAbstract</link>
            <description>Authors: Cole LE, Mann BJ, Shirey KA, Richard K, Yang Y, Gearhart PJ, Chesko KL, Viscardi RM, Vogel SN
    Immunization with Ft-LPS provokes an antigen-specific, B-1a cell-derived antibody response that protects WT mice against an otherwise lethal challenge with Ft LVS. However, this same regimen offers limited protection to TLR2(-/-) mice, despite production of WT levels of anti-Ft-LPS antibodies. As Ft-LPS exhibits no TLR2 agonist activity, and macrophage-induced cytokine production in response to Ft LVS is overwhelmingly TLR2-dependent, we hypothesized that treatment of TLR2(-/-) mice with an alternative, MyD88-dependent TLR agonist would compensate for reduced recognition of Ft LVS in TLR2(-/-) mice and thereby, restore Ft-LPS-mediated protection. Administration of the nontoxic TLR4 ag...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111964</comments>
            <pubDate>Mon, 11 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111964</guid>        </item>
        <item>
            <title>Exchange protein directly activated by cAMP 1 (Epac1) is expressed in human neutrophils and mediates cAMP-dependent activation of the monomeric GTPase Rap1.</title>
            <link>http://www.medworm.com/index.php?rid=5111962&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21750123%26dopt%3DAbstract</link>
            <description>Authors: Dash-Koney M, Deevi RK, McFarlane C, Dib K
    Epac1 and Epac2 bind cAMP and mediate cAMP-dependent activation of Rap1. cAMP is produced in neutrophils in response to many chemoattractants. This second messenger plays a key role in the regulation of the functions of neutrophils. However, it is still not known whether Epacs are expressed in human neutrophils. We found that stimulation of PLB-985 cells differentiated into neutrophil-like cells, human neutrophils with 8CPT-2Me-cAMP (a selective activator of Epacs), or FK (a diterpene that augments the intracellular level of cAMP) led to GTP-loading of Rap1. Epac1 mRNA was expressed in UND and DF PLB-985 cells, but Epac1 protein was only detected in DF PLB-985 cells. In human neutrophils, the Epac1 transcript was present, and Epac1 pr...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111962</comments>
            <pubDate>Mon, 11 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111962</guid>        </item>
        <item>
            <title>Regulation of angiostatic chemokines driven by IL-12 and IL-27 in human tumors.</title>
            <link>http://www.medworm.com/index.php?rid=5111960&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21750124%26dopt%3DAbstract</link>
            <description>Authors: Airoldi I, Ribatti D
    Chemokines have pleiotropic effects in regulating immunity, angiogenesis, and tumor growth. CXC and CC chemokine families members and their receptors are able to exert a proangiogenic or an antiangiogenic effect in experimental models and in human tumors. In this review article, we have summarized literature data and our studies concerning the angiostatic activity of chemokines. Their angiostatic activity may be a result of a direct effect on the biological functions of endothelial cells and/or an effect on tumor cells inhibiting their capability to stimulate new blood vessel formation. Moreover, chemokines have a pro- and antitumor effect within the tumor microenvironment by regulating immune cell infiltration and its antitumor activities. We have focused...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111960</comments>
            <pubDate>Mon, 11 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111960</guid>        </item>
        <item>
            <title>Clusterin induces matrix metalloproteinase-9 expression via ERK1/2 and PI3K/Akt/NF-{kappa}B pathways in monocytes/macrophages.</title>
            <link>http://www.medworm.com/index.php?rid=5019328&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21742938%26dopt%3DAbstract</link>
            <description>Authors: Shim YJ, Kang BH, Jeon HS, Park IS, Lee KU, Lee IK, Park GH, Lee KM, Schedin P, Min BH
    Most solid tumor tissues possess a significant population of macrophages, which are known to be closely linked with tumor progression and metastasis. Clusterin has been reported to be overexpressed in various tumors and to have a tumor-promoting role. As clusterin induction and macrophage infiltration occur concurrently at the tumor site, it raises a possibility that clusterin may regulate the function of macrophages via facilitating ECM remodeling. Here, we demonstrate for the first time the expression of MMP-9 by clusterin in human primary monocytes as well as human and murine macrophage cell lines, THP-1, and Raw264.7. MMP-9 expression was accompanied by increased enzymatic activity, as r...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5019328</comments>
            <pubDate>Thu, 07 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5019328</guid>        </item>
        <item>
            <title>Natural killer cell-mediated response to human cytomegalovirus-infected macrophages is modulated by their functional polarization.</title>
            <link>http://www.medworm.com/index.php?rid=5019327&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21742939%26dopt%3DAbstract</link>
            <description>Authors: Romo N, Magri G, Muntasell A, Heredia G, BaÃ­a D, Angulo A, Guma M, LÃ³pez-Botet M
    MÎ¦ comprise a heterogeneous population of cells, which contribute to host defense and maintenance of immune homeostasis. MÎ¦ may be infected by human cytomegalovirus (HCMV), which has evolved different strategies to subvert the immune response. In the present study, we comparatively analyzed the natural killer (NK) cell response against HCMV (TB40E)-infected proinflammatory (M1) and antinflammatory (M2) MÎ¦, derived from autologous monocytes, cultured in the presence of GM-CSF and M-CSF, respectively. M1 MÎ¦ were more resistant to infection and secreted IL-6, TNF-Î±, IFN-Î±, and IL-12; by contrast, in HCMV-infected M2 MÎ¦, proinflammatory cytokines, IL-10, and IFN-Î± production were limited and...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5019327</comments>
            <pubDate>Thu, 07 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5019327</guid>        </item>
        <item>
            <title>Investigations on the pattern recognition molecule M-ficolin: quantitative aspects of bacterial binding and leukocyte association.</title>
            <link>http://www.medworm.com/index.php?rid=5019330&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21730084%26dopt%3DAbstract</link>
            <description>Authors: Kjaer TR, Hansen AG, SÃ¸rensen UB, Nielsen O, Thiel S, Jensenius JC
    M-ficolin is a PRM of the innate immune system, found in serum and associated with leukocytes. We used the soluble form to study specificity toward Gram-positive bacteria and characterized and quantified cell-associated M-ficolin. The binding of M-ficolin to capsulated and noncapsulated strains of Streptococcus agalactiae (GBS) and Staphylococcus aureus was investigated. We did not observe binding of M-ficolin to any of 13 serotypes of S. aureus. Dose-dependent binding of M-ficolin was demonstrated for all of the capsulated GBS strains. The binding was abolished by prior treatment of the bacteria with sialidase, indicating that sialic acid is the ligand for M-ficolin on these bacteria. GlcNAc could inhibit the...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5019330</comments>
            <pubDate>Mon, 04 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5019330</guid>        </item>
        <item>
            <title>Plasmacytoid dendritic cells and cancer.</title>
            <link>http://www.medworm.com/index.php?rid=5019329&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21730085%26dopt%3DAbstract</link>
            <description>Authors: Vermi W, Soncini M, Melocchi L, Sozzani S, Facchetti F
    Cancer develops in a complex microenvironment comprising cancer cells, stromal cells, and host immune cells with their soluble products. The counteracting host-protective and tumor-promoting roles of different immune cell populations have been elegantly clarified in the last decade by pertinent genetically modified mouse models. Among cells with a potential role in cancer immunity, PDCs might represent important players as a result of their capacity to bring together innate and adaptive immunity. This review summarizes current knowledge about the role of PDCs in cancer immunity. PDCs have been documented in primary and metastatic human neoplasms; however, the clinical significance of this finding is still unknown. Once int...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5019329</comments>
            <pubDate>Mon, 04 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5019329</guid>        </item>
        <item>
            <title>Editorial: Counting the carbs: a memory B cell makeover.</title>
            <link>http://www.medworm.com/index.php?rid=5019336&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21719461%26dopt%3DAbstract</link>
            <description>Authors: Treanor B, Cancro MP
    
    PMID: 21719461 [PubMed - in process] (Source: Journal of Leukocyte Biology)</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5019336</comments>
            <pubDate>Thu, 30 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5019336</guid>        </item>
        <item>
            <title>Editorial: Serine proteases, serpins, and neutropenia.</title>
            <link>http://www.medworm.com/index.php?rid=5019335&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21719462%26dopt%3DAbstract</link>
            <description>Authors: Dale DC
    
    PMID: 21719462 [PubMed - in process] (Source: Journal of Leukocyte Biology)</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5019335</comments>
            <pubDate>Thu, 30 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5019335</guid>        </item>
        <item>
            <title>Development of tolerogenic dendritic cells and regulatory T cells favors exponential bacterial growth and survival during early respiratory tularemia.</title>
            <link>http://www.medworm.com/index.php?rid=5019334&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21724804%26dopt%3DAbstract</link>
            <description>Authors: Periasamy S, Singh A, Sahay B, Rahman T, Feustel PJ, Pham GH, Gosselin EJ, Sellati TJ
    Tularemia is a vector-borne zoonosis caused by Ft, a Gram-negative, facultative intracellular bacterium. Ft exists in two clinically relevant forms, the European biovar B (holarctica), which produces acute, although mild, self-limiting infections, and the more virulent United States biovar A (tularensis), which is often associated with pneumonic tularemia and more severe disease. In a mouse model of tularemia, respiratory infection with the virulence-attenuated Type B (LVS) or highly virulent Type A (SchuS4) strain engenders peribronchiolar and perivascular inflammation. Paradoxically, despite an intense neutrophilic infiltrate and high bacterial burden, T(h)1-type proinflammatory cytokines (...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5019334</comments>
            <pubDate>Thu, 30 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5019334</guid>        </item>
        <item>
            <title>Monocytes differentiated with GM-CSF and IL-15 initiate Th17 and Th1 responses that are contact-dependent and mediated by IL-15.</title>
            <link>http://www.medworm.com/index.php?rid=5019333&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21724805%26dopt%3DAbstract</link>
            <description>Authors: Harris KM
    Distinct types of DCs are generated from monocytes using GM-CSF with IL-4 (IL4-DC) or IL-15 (IL15-DC). IL15-DCs are potent inducers of antigen-specific CD8(+) T cells, display a phenotype similar to CD14(+) cells commonly described in chronically inflamed tissues, and produce high levels of IL-1Î² and IL-15 in response to TLR4 stimulation. As these cytokines promote Th17 responses, which are also associated with inflammatory diseases, I hypothesized that TLR-primed IL15-DCs favor Th17 activation over IL4-DCs. Compared with IL4-DCs, IL15-DCs stimulated with TLR agonists secreted significantly higher concentrations of the Th17-promoting factors, IL-1Î², IL-6, IL-23, and CCL20, and lower levels of the Th1 cytokine, IL-12. In addition, IL15-DCs and not IL4-DCs up-regulat...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5019333</comments>
            <pubDate>Thu, 30 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5019333</guid>        </item>
        <item>
            <title>Specific expression of GPR56 by human cytotoxic lymphocytes.</title>
            <link>http://www.medworm.com/index.php?rid=5019332&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21724806%26dopt%3DAbstract</link>
            <description>Authors: Peng YM, van de Garde MD, Cheng KF, Baars PA, Remmerswaal EB, van Lier RA, Mackay CR, Lin HH, Hamann J
    We here report the existence of a new cluster of adhesion-GPCRs in human immune cells. Analysis of a comprehensive immune cell transcriptome dataset indicated that expression of the closely related receptors, GPR56, GPR97, and GPR114, is associated with single lymphocyte and granulocyte subsets. Applying flow cytometric analysis with newly generated mAb, we show that expression of GPR56 is restricted to cytotoxic NK and T lymphocytes, including CD8(+), CD4(+), and Î³Î´ T cells. Primary infection with human CMV, which generates a vast population of CD8(+) T cells with an effector phenotype, induced a strong increase in GPR56 expression in virus-specific CD8(+) T cells that rem...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5019332</comments>
            <pubDate>Thu, 30 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5019332</guid>        </item>
        <item>
            <title>Intestinal epithelial cell-derived integrin {alpha}{beta}6 plays an important role in the induction of regulatory T cells and inhibits an antigen-specific Th2 response.</title>
            <link>http://www.medworm.com/index.php?rid=5019331&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21724807%26dopt%3DAbstract</link>
            <description>This study aims to dissect the molecular mechanisms by which IECs and protein antigen induce functional tolerogenic DCs and Tregs. Expression of Î±vÎ²6 by gut epithelial cell-derived exosomes, its coupling with food antigen, and their relationship with the development of functional tolerogenic DCs and Tregs were examined by using in vitro and in vivo approaches. The results show that IECs up-regulated the integrin Î±vÎ²6 upon uptake of antigens. The epithelial cell-derived exosomes entrapped and transported Î±vÎ²6 and antigens to the extracellular environment. The uptake of antigens alone induced DCs to produce LTGFÎ², whereas exosomes carrying Î±vÎ²6/antigen resulted in the production of abundant, active TGF-Î² in DCs that conferred to DCs the tolerogenic properties. Furthermore, Î±vÎ²6/O...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5019331</comments>
            <pubDate>Thu, 30 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5019331</guid>        </item>
        <item>
            <title>Evaluation of the Bcl-2 family antagonist ABT-737 in collagen-induced arthritis.</title>
            <link>http://www.medworm.com/index.php?rid=5019337&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21719460%26dopt%3DAbstract</link>
            <description>In this study, we demonstrate that treatment of DBA/1 mice, prior to the onset of CIA with ABT-737, a BH3 mimetic targeting Bcl-2, Bcl-w, and Bcl-x(L), ameliorated disease development. In contrast, treatment of mice with ABT-737 in established CIA did not alter the course of disease. ABT-737 induced lymphopenia, however pathogenic lymphoid populations in CIA mice were less affected, as shown by relatively normal T and B cell responses to CII. NaÃ¯ve lymphocytes were highly sensitive to apoptosis after culture with ABT-737, but synovial macrophages and neutrophils were not. Mcl-1 was detected in synovial monocyte/macrophages and neutrophils and strikingly, its expression, rather than Bcl-2 and Bcl-x(L), increased in the affected paws and lymphoid organs of mice with CIA. These observations ...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5019337</comments>
            <pubDate>Wed, 29 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5019337</guid>        </item>
        <item>
            <title>Nuocytes: expanding the innate cell repertoire in type-2 immunity.</title>
            <link>http://www.medworm.com/index.php?rid=5019340&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21712394%26dopt%3DAbstract</link>
            <description>Authors: Barlow JL, McKenzie AN
    Activation and differentiation of the Th1 cell population lead to their production of the classical type-1 cytokines IFN-Î³, IL-2, and TNF-Î², thus promoting type-1 immunity. This is thought to occur via the ligation of TLRs by bacterial and viral products, which in turn, drive production of the essential Th1 cell differentiation factor, IL-12, by dendritic cells (DCs). Concurrent studies have been able to identify the effector cytokines produced by Th2 cells (IL-4, IL-5, IL-9, and IL-13) as being essential for parasitic immunity and also as essential factors in allergic asthma. However, the factors that are critical for initiation of the type-2 response remained obscure. Recently however, two critical observations have led to a more detailed understandi...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5019340</comments>
            <pubDate>Mon, 27 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5019340</guid>        </item>
        <item>
            <title>Rac2 is required for the formation of neutrophil extracellular traps.</title>
            <link>http://www.medworm.com/index.php?rid=5019339&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21712395%26dopt%3DAbstract</link>
            <description>Authors: Lim MB, Kuiper JW, Katchky A, Goldberg H, Glogauer M
    Neutrophils play a critical role as a first line of defense against invading pathogens. Recently, a new defense strategy of neutrophils was described, in which pathogens are trapped and killed by NETs. However, the exact underlying mechanisms leading to the formation of NETs remain elusive. Here, we explored the role of the Rac small GTPases in the formation of NETs using neutrophils that lack Rac1, Rac2, or both isoforms. Efficient NET formation was observed in WT and Rac1null neutrophils. In contrast, NET formation was markedly impaired in cells lacking Rac2 or both Rac2 and Rac1. The defect in NET formation in Rac2null cells was rescued by exogenous ROS sources, suggesting that Rac2-mediated ROS generation is required for...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5019339</comments>
            <pubDate>Mon, 27 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5019339</guid>        </item>
        <item>
            <title>IFN-{gamma} production by lung NK cells is critical for the natural resistance to pulmonary metastasis of B16 melanoma in mice.</title>
            <link>http://www.medworm.com/index.php?rid=5019338&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21712396%26dopt%3DAbstract</link>
            <description>Authors: Takeda K, Nakayama M, Sakaki M, Hayakawa Y, Imawari M, Ogasawara K, Okumura K, Smyth MJ
    NK cells are effector lymphocytes playing a critical role in the natural resistance against tumors. However, the precise mechanisms underlying NK cell-mediated natural resistance against tumor metastasis are still unrevealed. B16 cells, mouse melanoma cells, were resistant to freshly isolated NK cell-mediated killing; nevertheless, NK cells were critical for natural resistance against experimental lung metastasis of B16 cells. We found that lung metastasis was increased significantly in IFN-Î³(-/- )mice but not pfp(-/-), IFN-Î±R(-/-), or IL-12/IL-18(-/-) mice. Interestingly, freshly isolated lung NK cells, but not spleen or liver NK cells, displayed augmented IFN-Î³ production after B16 ino...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5019338</comments>
            <pubDate>Mon, 27 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5019338</guid>        </item>
        <item>
            <title>In vivo-transmigrated human neutrophils are resistant to antiapoptotic stimulation.</title>
            <link>http://www.medworm.com/index.php?rid=4971548&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21697259%26dopt%3DAbstract</link>
            <description>In this study, in vivo-transmigrated neutrophils (tissue neutrophils) were collected using a skin chamber technique and compared with blood neutrophils from the same donors with respect to regulation of cell death. Skin chamber fluid contained a variety of cytokines known to activate neutrophils and regulate their lifespan. Freshly prepared tissue neutrophils had elevated activity of caspase 3/7 but were fully viable; spontaneous cell death after in vitro culture was also similar between blood and tissue neutrophils. Whereas apoptosis of cultured blood neutrophils was delayed by soluble antiapoptotic factors (e.g., TLR ligands), tissue neutrophils were completely resistant to antiapoptotic stimulation, even though receptors were present and functional. In vitro transmigration of blood neut...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4971548</comments>
            <pubDate>Tue, 21 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4971548</guid>        </item>
        <item>
            <title>Technical Advance: Langerhans cells derived from a human cell line in a full-thickness skin equivalent undergo allergen-induced maturation and migration.</title>
            <link>http://www.medworm.com/index.php?rid=4971547&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21697260%26dopt%3DAbstract</link>
            <description>In this report, the construction of a functional, immunocompetent, full-thickness skin equivalent (SE) is described, consisting of an epidermal compartment containing keratinocytes, melanocytes, and human LCs derived from the MUTZ-3 cell line (MUTZ-LC) and a fibroblast-populated dermal compartment. The CD1a(+)Langerin(+)HLA-DR(+) MUTZ-LCs populate the entire epidermis at a similar density to that found in native skin. Exposure of the SE to subtoxic concentrations of the allergens NiSO(4) and resorcinol resulted in LC migration out of the epidermis toward the fibroblast-populated dermal compartment. A significant dose-dependent up-regulation of the DC maturation-related CCR7 and IL-1Î² transcripts and of CD83 at the protein level upon epidermal exposure to both allergens was observed, indic...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4971547</comments>
            <pubDate>Tue, 21 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4971547</guid>        </item>
        <item>
            <title>Apple polyphenols require T cells to ameliorate dextran sulfate sodium-induced colitis and dampen proinflammatory cytokine expression.</title>
            <link>http://www.medworm.com/index.php?rid=4971549&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21693591%26dopt%3DAbstract</link>
            <description>In this study, treatment with APP was investigated to ameliorate chemically induced colitis. Oral but not peritoneal administration of APP during colitis induction significantly protected C57BL/6 mice against disease, as evidenced by the lack of weight loss, colonic inflammation, and shortening of the colon. APP administration dampened the mRNA expression of IL-1Î², TNF-Î±, IL-6, IL-17, IL-22, CXCL9, CXCL10, CXCL11, and IFN-Î³ in the colons of mice with colitis. APP-mediated protection requires T cells, as protection was abated in Rag-1(-/-) or TCRÎ±(-/-) mice but not in IL-10(-/-), IRF-1(-/-), Î¼ MT, or TCRÎ´(-/-) mice. Administration of APP during colitis to TCRÎ±(-/-) mice actually enhanced proinflammatory cytokine expression, further demonstrating a requirement for TCRÎ±Î² cells in APP...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4971549</comments>
            <pubDate>Mon, 20 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4971549</guid>        </item>
        <item>
            <title>SHIP-deficient, alternatively activated macrophages protect mice during DSS-induced colitis.</title>
            <link>http://www.medworm.com/index.php?rid=4971552&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21685246%26dopt%3DAbstract</link>
            <description>This study supports our hypothesis by demonstrating that SHIP-deficient, M2a mÏ• are protective in this murine model of acute intestinal inflammation. Adoptive transfer of M2a mÏ• to patients with IBDs offers a promising, new strategy for treatment that may be particularly useful in patients who are otherwise refractory to conventional therapies.
    PMID: 21685246 [PubMed - as supplied by publisher] (Source: Journal of Leukocyte Biology)</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4971552</comments>
            <pubDate>Thu, 16 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4971552</guid>        </item>
        <item>
            <title>Lutzomyia longipalpis saliva drives apoptosis and enhances parasite burden in neutrophils.</title>
            <link>http://www.medworm.com/index.php?rid=4971551&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21685247%26dopt%3DAbstract</link>
            <description>Authors: Prates DB, AraÃºjo-Santos T, Luz NF, Andrade BB, FranÃ§a-Costa J, Afonso L, ClarÃªncio J, Miranda JC, Bozza PT, Dosreis GA, Brodskyn C, Barral-Netto M, Borges VD, Barral A
    Neutrophils are considered the host's first line of defense against infections and have been implicated in the immunopathogenesis of Leishmaniasis. Leishmania parasites are inoculated alongside vectors' saliva, which is a rich source of pharmacologically active substances that interfere with host immune response. In the present study, we tested the hypothesis that salivary components from Lutzomyia longipalpis, an important vector of visceral Leishmaniasis, enhance neutrophil apoptosis. Murine inflammatory peritoneal neutrophils cultured in the presence of SGS presented increased surface expression of FasL a...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4971551</comments>
            <pubDate>Thu, 16 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4971551</guid>        </item>
        <item>
            <title>Toll-like receptor activation and hypoxia use distinct signaling pathways to stabilize hypoxia-inducible factor 1{alpha} (HIF1A) and result in differential HIF1A-dependent gene expression.</title>
            <link>http://www.medworm.com/index.php?rid=4971550&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21685248%26dopt%3DAbstract</link>
            <description>Authors: Jantsch J, Wiese M, SchÃ¶del J, Castiglione K, GlÃ¤sner J, Kolbe S, Mole D, Schleicher U, Eckardt KU, Hensel M, Lang R, Bogdan C, Schnare M, Willam C
    HIF1A is a transcription factor that plays a central role for the adaptation to tissue hypoxia and for the inflammatory response of myeloid cells, including DCs. HIF1A is stabilized by hypoxia but also by TLR ligands under normoxic conditions. The underlying signaling events leading to the accumulation of HIF1A in the presence of oxygen are still poorly understood. Here, we show that in contrast to hypoxic stabilization of HIF1A, normoxic, TLR-mediated HIF1A accumulation in DCs follows a different pathway that predominantly requires MYD88-dependent NF-ÎºB activity. The TLR-induced HIF1A controls a subset of proinflammatory genes ...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4971550</comments>
            <pubDate>Thu, 16 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4971550</guid>        </item>
        <item>
            <title>Systemic mast cell degranulation increases mortality during polymicrobial septic peritonitis in mice.</title>
            <link>http://www.medworm.com/index.php?rid=4922904&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21653231%26dopt%3DAbstract</link>
            <description>Authors: Seeley EJ, Sutherland RE, Kim SS, Wolters PJ
    MCs are required for an effective host response during septic peritonitis. Local MC degranulation facilitates neutrophil recruitment, activation, and bacterial killing. However, the role of MCs located distant from the site of infection is unknown. We studied the temporal and spacial degranulation of MCs following CLP-induced septic peritonitis. The functional importance of systemic MC degranulation during infection was evaluated by compartment-specific MC reconstitution. Serum histamine, reflecting MC degranulation, was elevated 4 h after onset of septic peritonitis. Histologic examination revealed progressive MC degranulation in select tissues during the first 24 h of infection. MC-deficient Wsh mice, reconstituted only in the per...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4922904</comments>
            <pubDate>Mon, 06 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4922904</guid>        </item>
        <item>
            <title>Glia maturation factor-{gamma} mediates neutrophil chemotaxis.</title>
            <link>http://www.medworm.com/index.php?rid=4922903&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21653232%26dopt%3DAbstract</link>
            <description>Authors: Aerbajinai W, Liu L, Chin K, Zhu J, Parent CA, Rodgers GP
    Chemotaxis is fundamental to the directional migration of neutrophils toward endogenous and exogenous chemoattractants. Recent studies have demonstrated that ADF/cofilin superfamily members play important roles in reorganizing the actin cytoskeleton by disassembling actin filaments. GMFG, a novel ADF/cofilin superfamily protein that is expressed in inflammatory cells, has been implicated in regulating actin reorganization in microendothelial cells, but its function in neutrophils remains unclear. Here, we show that GMFG is an important regulator for cell migration and polarity in neutrophils. Knockdown of endogenous GMFG impaired fMLF- and IL-8 (CXCL8)-induced chemotaxis in dHL-60 cells. GMFG knockdown attenuated the fo...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4922903</comments>
            <pubDate>Mon, 06 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4922903</guid>        </item>
        <item>
            <title>Protein kinase C{delta} is a critical component of Dectin-1 signaling in primary human monocytes.</title>
            <link>http://www.medworm.com/index.php?rid=4922902&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21653233%26dopt%3DAbstract</link>
            <description>In this study, we examined the involvement of various pattern recognition receptors and found that Dectin-1 is the primary receptor for zymosan stimulation of O(2)(.-) via NADPH oxidase in human monocytes, whereas Dectin-1 and CR3 mediate the activation by ZOP. Further studies identified Syk and Src as important signaling components downstream of Dectin-1 and additionally identified PKCÎ´ as a novel downstream signaling component for zymosan-induced O(2)(.-) as well as phagocytosis. Our results show that Syk and Src association with Dectin-1 is dependent on PKCÎ´ activity and expression and demonstrate direct binding between Dectin-1 and PKCÎ´. Finally, our data show that PKCÎ´ and Syk but not Src are required for Dectin-1-mediated phagocytosis. Taken together, our data identify Dectin-1 a...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4922902</comments>
            <pubDate>Mon, 06 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4922902</guid>        </item>
        <item>
            <title>17(R)-Resolvin D1 differentially regulates TLR4-mediated responses of primary human macrophages to purified LPS and live E. coli.</title>
            <link>http://www.medworm.com/index.php?rid=4922899&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21653234%26dopt%3DAbstract</link>
            <description>Authors: Palmer CD, Mancuso CJ, Weiss JP, Serhan CN, Guinan EC, Levy O
    Detection and clearance of bacterial infection require balanced effector and resolution signals to avoid chronic inflammation. Detection of GNB LPS by TLR4 on mÏ• induces inflammatory responses, contributing to chronic inflammation and tissue injury. LXs and Rvs are endogenous lipid mediators that enhance resolution of inflammation, and their actions on primary human mÏ• responses toward GNB are largely uncharacterized. Here, we report that LXA(4), LXB(4), and RvD1, tested at 0.1-1 Î¼M, inhibited LPS-induced TNF production from primary human mÏ•, with ATL and 17(R)-RvD1, demonstrating potent inhibition at 0.1 Î¼M. In addition, 17(R)-RvD1 inhibited LPS-induced primary human mÏ• production of IL-7, IL-12p70, GM-CSF, I...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4922899</comments>
            <pubDate>Mon, 06 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4922899</guid>        </item>
        <item>
            <title>Modulation of regulatory T cell-Th17 balance by plasmacytoid dendritic cells.</title>
            <link>http://www.medworm.com/index.php?rid=4922898&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21653235%26dopt%3DAbstract</link>
            <description>In this study, we have analyzed the role of pDCs versus cDCs on Treg responses and underlined that pDCs have an intrinsic, unique capacity to induce IL-17 secretion from T cells. We showed in rats that FoxP3(+) Tregs were able to secrete IL-17 only when stimulated by allogeneic, mature pDCs but not cDCs. In addition, in rats and mice, mature pDCs but not cDCs inhibited in vitro Treg-suppressive functions and in the presence of Tregs, supported Th17 differentiation from naive T cells through secretion of high amounts of IL-6. These data suggest an important role for pDCs in modulating or switching Treg function and allowing Th17 differentiation.
    PMID: 21653235 [PubMed - as supplied by publisher] (Source: Journal of Leukocyte Biology)</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4922898</comments>
            <pubDate>Mon, 06 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4922898</guid>        </item>
        <item>
            <title>Specificity of eicosanoid production depends on the TLR-4-stimulated macrophage phenotype.</title>
            <link>http://www.medworm.com/index.php?rid=4922897&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21653236%26dopt%3DAbstract</link>
            <description>Authors: Norris PC, Reichart D, Dumlao DS, Glass CK, Dennis EA
    Eicosanoid metabolism differs in profile and quantity between macrophages of different tissue origin and method of elicitation, as well as between primary and immortalized macrophages after activation with inflammatory stimuli. Using a lipidomic approach, we comprehensively analyzed the eicosanoids made by murine RPMs, TGEMs, BMDM, and the macrophage-like cell line RAW after stimulation with the TLR-4-specific agonist KLA. Direct correlation among total COX metabolites, COX side-products (11-HETE, 15-HETE), COX-2 mRNA, and protein at 8 h was found when comparing each cell type. Comprehensive qPCR analysis was used to compare relative transcript levels between the terminal prostanoid synthases themselves as well as between e...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4922897</comments>
            <pubDate>Mon, 06 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4922897</guid>        </item>
        <item>
            <title>Technical Advance:Immunophenotypical characterization of human neutrophil differentiation.</title>
            <link>http://www.medworm.com/index.php?rid=4922896&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21653237%26dopt%3DAbstract</link>
            <description>Authors: Jensen HM, Jendholm J, Fossum A, Porse B, Borregaad N, Theilgaard-MÃ¶nch K
    The current study reports a flow cytometry-based protocol for the prospective purification of human BM populations representing six successive stages of terminal neutrophil differentiation, including early promyelocytes and late promyelocytes, myelocytes, metamyelocytes, band cells, and PMN neutrophilic granulocyte. Validation experiments revealed a high purity of each bone marrow population and biological meaningful expression profiles for marker genes of neutrophil differentiation at a hitherto unprecedented resolution. Hence, the present protocol should be useful for studying neutrophil differentiation in vivo in the human setting and constitutes an important alternative to models that are based on i...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4922896</comments>
            <pubDate>Mon, 06 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4922896</guid>        </item>
        <item>
            <title>Technical Advance:Soluble OX40 molecule mimics regulatory T cell modulatory activity on Fc{varepsilon}RI-dependent mast cell degranulation.</title>
            <link>http://www.medworm.com/index.php?rid=4922895&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21653238%26dopt%3DAbstract</link>
            <description>Authors: Sibilano R, Gri G, Frossi B, Tripodo C, Suzuki R, Rivera J, Macdonald AS, Pucillo CE
    Tregs play a central role in modulating FcÎµRI-dependent MC effector functions in the course of the allergic response. Cellular interaction depends on the constitutive expression of OX40 on Tregs and the OX40L counterpart on MCs. Study of OX40L signaling on MCs is hampered by the need of a highly purified molecule, which triggers OX40L specifically. We now report that sOX40 mimics the physiological activity of Treg interaction by binding to activated MCs. When treated with sOX40, activated MCs showed decreased degranulation and Ca(++) influx, whereas PLC-Î³2 phosphorylation remained unaffected. Once injected into experimental animals, sOX40 not only located within the endothelium but also in p...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4922895</comments>
            <pubDate>Mon, 06 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4922895</guid>        </item>
        <item>
            <title>Nod-like receptors in intestinal homeostasis, inflammation, and cancer.</title>
            <link>http://www.medworm.com/index.php?rid=4922894&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21653239%26dopt%3DAbstract</link>
            <description>Authors: Werts C, Rubino S, Ling A, Girardin SE, Philpott DJ
    NLRs have been shown in a number of models to protect against microbial infection through their ability to participate in &quot;pattern recognition&quot; and their triggering of inflammatory pathways to control infection. Over the past few years, however, the role of NLRs, especially Nod1, Nod2, and NLRP3, in intestinal homeostasis has been highlighted. Indeed, these specific NLRs have been implicated in IBD, in particular, the association of Nod2 with CD, yet a clear understanding of how dysfunctional NLR activation leads to aberrant inflammation is still the focus of much investigation. In this review, we will examine how NLRs participate in the maintenance of gut homeostasis and how upset of this regulation can tip the balance towar...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4922894</comments>
            <pubDate>Mon, 06 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4922894</guid>        </item>
        <item>
            <title>Frequencies of FoxP3+ naive T cells are related to both viral load and naive T cell proliferation responses in HIV disease.</title>
            <link>http://www.medworm.com/index.php?rid=4922893&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21653240%26dopt%3DAbstract</link>
            <description>Authors: Rodriguez B, Bazdar DA, Funderburg N, Asaad R, Luciano AA, Yadavalli G, Kalayjian RC, Lederman MM, Sieg SF
    HIV infection results in depletion and dysfunction of naÃ¯ve CD4(+) T cells. The mechanisms underlying these deficiencies are not understood. We investigated the frequencies of CD4(+) naÃ¯ve subsets in HIV disease as defined by expression of CD25 and/or FoxP3 and the relationship of these frequencies to naÃ¯ve T cell proliferation function. We observed increased proportions of CD25(+)FoxP3(+) and CD25(+)FoxP3(-) cells and decreased proportions of CD25(-)FoxP3(-) cells within the naÃ¯ve CD4(+) cell compartment from HIV-infected persons compared with findings in healthy donors. These perturbations were related to higher plasma HIV RNA levels but not with higher immune activ...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4922893</comments>
            <pubDate>Mon, 06 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4922893</guid>        </item>
        <item>
            <title>The historical milestones in the understanding of leukocyte biology initiated by Elie Metchnikoff.</title>
            <link>http://www.medworm.com/index.php?rid=4922914&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21628329%26dopt%3DAbstract</link>
            <description>Authors: Cavailon JM
    Progress in science is made with key discoveries, correct analyses, wrong statements, and disputes within the scientific community. Despite scientific controversies, Elie Metchnikoff has allowed the theory of phagocytes to triumph. Starting his career as a zoologist, Metchnikoff became a pathologist, beautifully defining the role of monocytes, macrophages, and neutrophils during inflammation and innate immunity. The discoveries of immune cells were made by other outstandings scientists, such as Paul Ehrlich, whose key contributions to humoral immunity led him to share the Nobel Prize with Metchnikoff. Ludwig Aschoff grouped certain cells under the term RES, according to their propensity for absorbing and storing vital stains. This classification was not always a so...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4922914</comments>
            <pubDate>Thu, 02 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4922914</guid>        </item>
        <item>
            <title>Gene expression analysis of dendritic cells that prevent diabetes in NOD mice: analysis of chemokines and costimulatory molecules.</title>
            <link>http://www.medworm.com/index.php?rid=4922911&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21628331%26dopt%3DAbstract</link>
            <description>Authors: Morel PA, Srinivas M, Turner MS, Fuschiotti P, Munshi R, Bahar I, Feili-Hariri M, Ahrens ET
    We have demonstrated previously that BM-derived DCs can prevent diabetes development and halt progression of insulitis in NOD mice, the mouse model of type 1 diabetes. The DC population that was most effective in this therapy had a mature phenotype, expressed high levels of costimulatory molecules, and secreted low levels of IL-12p70. The protective DC therapy induced Treg and Th2 cells in vitro and in vivo. Microarray analysis of therapeutic and nontherapeutic DC populations revealed differences in the expression of OX40L, CD200, Ym-1, CCL2, and CCL5, which could play important roles in the observed DC-mediated therapy. The unique pattern of costimulatory molecules and chemokines expre...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4922911</comments>
            <pubDate>Thu, 02 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4922911</guid>        </item>
        <item>
            <title>Susceptibility to tuberculosis is associated with TLR1 polymorphisms resulting in a lack of TLR1 cell surface expression.</title>
            <link>http://www.medworm.com/index.php?rid=4922905&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21642391%26dopt%3DAbstract</link>
            <description>Authors: Uciechowski P, Imhoff H, Lange C, Meyer CG, Browne EN, Kirsten DK, SchrÃ¶der AK, Schaaf B, Al-Lahham A, Reinert RR, Reiling N, Haase H, Hatzmann A, Fleischer D, Heussen N, Kleines M, Rink L
    Human TLR1 plays an important role in host defense against Mycobacterium tuberculosis. Our aim was to analyze the association of the loss of TLR1 surface expression and TLR1 SNPs with susceptibility to TB. TLR1neg and TLR1pos cells from healthy individuals were identified by flow cytometry and compared by sequencing. TLR1 expression was measured using quantitative real-time PCR and immunoblotting. TLR1 SNP analyses of healthy individuals and TB patients from EU-C and Ghana were performed, and association of the TLR1 genotypes with increased risk of developing TB was statistically evaluated....</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4922905</comments>
            <pubDate>Thu, 02 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4922905</guid>        </item>
        <item>
            <title>Editorial: Interfering with B cell immunity.</title>
            <link>http://www.medworm.com/index.php?rid=4922907&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21628334%26dopt%3DAbstract</link>
            <description>Authors: Harris JE, Marshak-Rothstein A
    
    PMID: 21628334 [PubMed - in process] (Source: Journal of Leukocyte Biology)</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4922907</comments>
            <pubDate>Tue, 31 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4922907</guid>        </item>
        <item>
            <title>Editorial: Cytohesin-1, on the tail of two integrins.</title>
            <link>http://www.medworm.com/index.php?rid=4922906&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21628335%26dopt%3DAbstract</link>
            <description>Authors: Hyduk SJ, Cybulsky MI
    
    PMID: 21628335 [PubMed - in process] (Source: Journal of Leukocyte Biology)</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4922906</comments>
            <pubDate>Tue, 31 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4922906</guid>        </item>
        <item>
            <title>Improved host defense against septic peritonitis in mice lacking MyD88 and TRIF is linked to a normal interferon response.</title>
            <link>http://www.medworm.com/index.php?rid=4922913&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21628330%26dopt%3DAbstract</link>
            <description>Authors: Reim D, Rossmann-Bloeck T, Jusek G, Prazeres da Costa O, Holzmann B
    The signaling adapters MyD88 and TRIF are engaged by TLRs and/or receptors of the IL-1 family and are considered important for innate immune responses that combat bacterial infections. Here, the consequences of a combined MyD88 and TRIF deficiency for the innate immune response against severe septic peritonitis was examined. We demonstrate that Myd88(-/-);Trif(Lps2/Lps2)mice had markedly reduced bacterial numbers in the peritoneal cavity and peripheral blood, indicating that bacterial clearance in this model is improved in the absence of MyD88/TRIF signals. Survival of Myd88(-/-); Trif(Lps2/Lps2) mice was improved significantly. The lack of MyD88/TRIF signaling prevented the excessive production of inflammator...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4922913</comments>
            <pubDate>Mon, 30 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4922913</guid>        </item>
        <item>
            <title>Suppressor of cytokine signaling (SOCS)1 is a key determinant of differential macrophage activation and function.</title>
            <link>http://www.medworm.com/index.php?rid=4922909&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21628332%26dopt%3DAbstract</link>
            <description>Authors: Whyte CS, Bishop ET, RÃ¼ckerl D, Gaspar-Pereira S, Barker RN, Allen JE, Rees AJ, Wilson HM
    Macrophages become activated by their environment and develop polarized functions, classically activated (M1) macrophages eliminate pathogens but can cause tissue injury, whereas alternatively activated (M2) macrophages promote healing and repair. Mechanisms directing polarized activation, especially in vivo, are not understood completely, and here, we examined the role of SOCS proteins. M2 macrophages activated in vitro or elicited by implanting mice i.p. with the parasitic nematode Brugia malayi display a selective and IL-4-dependent up-regulation of SOCS1 but not SOCS3. Using siRNA-targeted knockdown in BMDM, we reveal that the enhanced SOCS1 is crucial for IL-4-induced M2 characteris...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4922909</comments>
            <pubDate>Mon, 30 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4922909</guid>        </item>
        <item>
            <title>Reciprocal regulation of CXCR4 and CXCR7 in intestinal mucosal homeostasis and inflammatory bowel disease.</title>
            <link>http://www.medworm.com/index.php?rid=4922908&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21628333%26dopt%3DAbstract</link>
            <description>In conclusion, the present study suggests that the interplay between CXCL12 and its receptors affects homeostasis and inflammation in the intestinal mucosa.
    PMID: 21628333 [PubMed - as supplied by publisher] (Source: Journal of Leukocyte Biology)</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4922908</comments>
            <pubDate>Mon, 30 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4922908</guid>        </item>
        <item>
            <title>Endotoxin-induced uveitis is primarily dependent on radiation-resistant cells and on MyD88 but not TRIF.</title>
            <link>http://www.medworm.com/index.php?rid=4877123&amp;cid=s_37898_19_f&amp;fid=37898&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21610198%26dopt%3DAbstract</link>
            <description>Authors: Kezic J, Taylor S, Gupta S, Planck SR, Rosenzweig HL, Rosenbaum JT
    TLR4 activation by LPS (endotoxin) is mediated by the MyD88 and TRIF intracellular signaling pathways. We determined the relative activation of these pathways in murine ocular tissue after LPS exposure. Additionally, we explored whether BM-derived or non-BM-derived cells were the major contributors to EIU. Mice deficient in TRIF or MyD88 and their congenic (WT) controls received 250 ng ultrapure LPS ivt at 0 h. Ocular inflammation was assessed by histological analysis at 4, 6, and 24 h, and additionally, in MyD88(-/-) mice, intravital microscopy was performed at 4 h and 6 h to assess adherent, rolling, and infiltrating cells in the iris vasculature and tissue. Cytokines associated with the MyD88 and TRIF intrac...</description>
            <author>Journal of Leukocyte Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4877123</comments>
            <pubDate>Mon, 23 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4877123</guid>        </item>
    </channel>
</rss>

