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        <title>Clinical and Experimental Immunology via MedWorm.com</title>
        <description>MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest items from the 'Clinical and Experimental Immunology' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Clinical+and+Experimental+Immunology&t=Clinical+and+Experimental+Immunology&s=Search&f=source]]></link>
        <lastBuildDate>Sat, 20 Mar 2010 13:39:21 +0100</lastBuildDate>
        <item>
            <title>An imbalance in mucosal cytokine profile causes transient intestinal inflammation following an animal's first exposure to faecal bacteria and antigens</title>
            <link>http://www.medworm.com/index.php?rid=3371221&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2010.04140.x</link>
            <description>This study examined the effects of faecal bacteria and antigen exposure on the intestinal mucosal and systemic immune system in healthy axenic mice. Axenic wild-type mice were inoculated orally with a crude faecal slurry solution derived from conventionally raised mice and were analysed prior to and then at days 3, 7, 14 and 28 post-treatment. Ingestion of faecal slurry resulted in a transient, early onset of proinflammatory interferon (IFN)-[gamma], tumour necrosis factor (TNF)-[alpha] and interleukin (IL)-17 response that was maximal at day 3. In contrast, the transient release of the anti-inflammatory cytokines IL-10 and IL-4 occurred later and was maximal at day 7. Both responses subsided by day 14. This early cytokine imbalance was associated with a brief rise in colonic and caecal hi...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3371221</comments>
            <pubDate>Wed, 17 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3371221</guid>        </item>
        <item>
            <title>Activation of signal transducer and activator of transcription-1 (STAT-1) and differential expression of interferon-&amp;#x03B3; and anti-inflammatory proteins in pelvic ileal pouches for ulcerative colitis and familial adenomatous polyposis</title>
            <link>http://www.medworm.com/index.php?rid=3371231&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04088.x</link>
            <description>Pouchitis after total rectocolectomy is the most common complication of ulcerative colitis (UC). The immunological mechanisms involved in the genesis of pouchitis are unclear. Therefore, we evaluated the inflammatory activity in normal ileal pouch mucosa by determining signal transducers and activators of transcription (STAT-1) activation and cytokine expression in patients operated for UC and familial adenomatous polyposis (FAP). Eighteen asymptomatic patients, who underwent total rectocolectomy and J pouch, were evaluated: nine with UC and nine with FAP. The activation of STAT-1 and cytokine expression were determined by immunoblot of total protein extracts from pouch mucosal biopsies. The absence of pouchitis was assessed by clinical, histological and endoscopic parameters, according to...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3371231</comments>
            <pubDate>Tue, 16 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3371231</guid>        </item>
        <item>
            <title>Tolerance induction after specific immunotherapy with pollen allergoids adjuvanted by monophosphoryl lipid A in children</title>
            <link>http://www.medworm.com/index.php?rid=3371230&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2010.04106.x</link>
            <description>Specific immunotherapy (SIT) is a well-established and clinically effective treatment for allergic diseases. A pollen allergoid formulated with the T helper type 1 (Th1)-inducing adjuvant monophosphoryl lipid A (MPL) facilitates short-term SIT. Little is known about mechanisms of tolerance induction in this setting. In a prospective study, 34 patients allergic to grass pollen (25 male, nine female, median age 10·2 years) received a total of 44 SIT courses (20 in the first, 24 in the second) with MPL-adjuvanted pollen allergoids. Immunogenicity was measured by levels of specific immunoglobulin G (IgGgrass) and IgG4grass by antibody blocking properties on basophil activation, and by induction of CD4+, CD25+ and forkhead box P3 (FoxP3+) regulatory T cells (Treg). Specific IgG and IgG4 levels...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3371230</comments>
            <pubDate>Tue, 16 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3371230</guid>        </item>
        <item>
            <title>Various effects of different probiotic strains in allergic disorders: an update from laboratory and clinical data</title>
            <link>http://www.medworm.com/index.php?rid=3371229&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2010.04109.x</link>
            <description>Epidemiological data show that allergic children have a different intestinal flora from healthy children with higher levels of Clostridia and lower levels of Bifidobacteria. Nonetheless, Bifidobacteria and Lactobacilli are found more commonly in the composition of the intestinal flora of non-allergic children. Probiotics are ingested live microbes that can modify intestinal microbial populations in a way that benefits the host and they are represented mainly by Lactobacilli. Enhanced presence of probiotic bacteria in the intestinal microbiota is found to correlate with protection against atopy. There is also very promising evidence to recommend the addition of probiotics to foods for the prevention and treatment of allergic diseases. Clinical improvement, especially in allergic rhinitis an...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3371229</comments>
            <pubDate>Tue, 16 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3371229</guid>        </item>
        <item>
            <title>A role for human endogenous retrovirus-K (HML-2) in rheumatoid arthritis: investigating mechanisms of pathogenesis</title>
            <link>http://www.medworm.com/index.php?rid=3371228&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2010.04110.x</link>
            <description>Human endogenous retroviruses (HERVs) are remnants of ancient retroviral infections within the human genome. These molecular fossils draw parallels with present-day exogenous retroviruses and have been linked previously with immunopathology within rheumatoid arthritis (RA). Mechanisms of pathogenesis for HERV-K in RA such as molecular mimicry were investigated. To clarify a role for HERVs in RA, potential autoantigens implicated in autoimmunity were scanned for sequence identity with retroviral epitopes. Short retroviral peptides modelling shared epitopes were synthesized, to survey anti-serum of RA patients and disease controls. A novel real-time polymerase chain reaction (PCR) assay was also developed to quantify accurately levels of HERV-K (HML-2) gag expression, relative to normalized ...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3371228</comments>
            <pubDate>Tue, 16 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3371228</guid>        </item>
        <item>
            <title>Ketamine reduces inducible superoxide generation in human neutrophils in vitro by modulating the p38 mitogen-activated protein kinase (MAPK)-mediated pathway</title>
            <link>http://www.medworm.com/index.php?rid=3371227&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2010.04111.x</link>
            <description>Many cellular stresses and inflammatory stimuli can activate p38 mitogen-activated protein kinase (MAPK), a serine/threonine kinase in the MAPK family. The different stimuli act via different receptors or signalling pathways to induce phosphorylation of the cytosolic protein p47phox, one subunit of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. Formyl[ndash]methionyl[ndash]leucyl[ndash]phenylalanine (fMLP) has been shown to induce the p38 MAPK phosphorylation during the respiratory burst in human neutrophils. Here, we show that treatment with S(+)-ketamine or R(-)-ketamine at different concentrations (50, 100, 200, 400 µM) reduced fMLP-induced superoxide anion generation and p47phox phosphorylation in neutrophils in a concentration-dependent manner (y = [minus]0·093x + ...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3371227</comments>
            <pubDate>Tue, 16 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3371227</guid>        </item>
        <item>
            <title>Mitigation of septic shock in mice and rhesus monkeys by human chorionic gonadotrophin-related oligopeptides</title>
            <link>http://www.medworm.com/index.php?rid=3371226&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2010.04112.x</link>
            <description>The marked improvement of several immune-mediated inflammatory diseases during pregnancy has drawn attention to pregnancy hormones as potential therapeutics for such disorders. Low molecular weight fractions derived from the pregnancy hormone human chorionic gonadotrophin (hCG) have remarkable potent immunosuppressive effects in mouse models of diabetes and septic shock. Based on these data we have designed a set of oligopeptides related to the primary structure of hCG and tested these in models of septic shock in mice and rhesus monkeys. We demonstrate that mice exposed to lipopolysaccharide (LPS) and treated subsequently with selected tri-, tetra-, penta- and hepta-meric oligopeptides (i.e. MTR, VVC, MTRV, LQGV, AQGV, VLPALP, VLPALPQ) are protected against fatal LPS-induced septic shock....</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3371226</comments>
            <pubDate>Tue, 16 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3371226</guid>        </item>
        <item>
            <title>Cyclophilin&amp;#x2013;CD147 interactions: a new target for anti-inflammatory therapeutics</title>
            <link>http://www.medworm.com/index.php?rid=3371225&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2010.04115.x</link>
            <description>CD147 is a widely expressed plasma membrane protein that has been implicated in a variety of physiological and pathological activities. It is best known for its ability to function as extracellular matrix metalloproteinase inducer (hence the other name for this protein, EMMPRIN), but has also been shown to regulate lymphocyte responsiveness, monocarboxylate transporter expression and spermatogenesis. These functions reflect multiple interacting partners of CD147. Among these CD147-interacting proteins cyclophilins represent a particularly interesting class, both in terms of structural considerations and potential medical implications. CD147 has been shown to function as a signalling receptor for extracellular cyclophilins A and B and to mediate chemotactic activity of cyclophilins towards ...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3371225</comments>
            <pubDate>Tue, 16 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3371225</guid>        </item>
        <item>
            <title>Altered expression of signalling lymphocyte activation molecule (SLAM) family receptors CS1 (CD319) and 2B4 (CD244) in patients with systemic lupus erythematosus</title>
            <link>http://www.medworm.com/index.php?rid=3371224&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2010.04116.x</link>
            <description>In this study, we have investigated the expression and alternative splicing of CS1 and 2B4 in immune cells from SLE patients. The surface expression of CS1 and 2B4 on total peripheral blood mononuclear cells (PBMCs), T, B, natural killer (NK) cells and monocytes in 45 patients with SLE and 30 healthy individuals was analysed by flow cytometry. CS1-positive B cell population was increased significantly in SLE patients. Because CS1 is a self-ligand and homophilic interaction of CS1 induces B cell proliferation and autocrine cytokine secretion, this could account for autoreactive B cell proliferation in SLE. The proportion of NK cells and monocytes expressing 2B4 on their surface was significantly lower in patients with SLE compared to healthy controls. Our study demonstrated altered expressi...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3371224</comments>
            <pubDate>Tue, 16 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3371224</guid>        </item>
        <item>
            <title>Coupled regulation of interleukin-12 receptor beta-1 of CD8+ central memory and CCR7-negative memory T cells in an early alloimmunity in liver transplant recipients</title>
            <link>http://www.medworm.com/index.php?rid=3371223&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2010.04117.x</link>
            <description>In conclusion, this work demonstrated that the IL-12R[beta]1+ cells of TCM and CNS are regulated in a tightly coupled manner and that expression levels of IL-12R[beta]1+ TCM play a crucial role in controlling allo- and infectious immunity. (Source: Clinical and Experimental Immunology)</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3371223</comments>
            <pubDate>Tue, 16 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3371223</guid>        </item>
        <item>
            <title>Toluene diisocyanate (TDI) regulates haem oxygenase-1/ferritin expression: implications for toluene diisocyanate-induced asthma</title>
            <link>http://www.medworm.com/index.php?rid=3371222&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2010.04118.x</link>
            <description>In this study of toluene diisocyanate (TDI)-OA, we found identical findings with increased transferrin and decreased ferritin levels in the serum of patients with TDI-OA. To elucidate whether diisocyanate suppresses FTL synthesis directly, we tested the effect of TDI on the FTL synthesis in A549 cells, a human airway epithelial cell line. We found that haem oxygenase-1 as well as FTL was suppressed by treatment with TDI in dose- and time-dependent manners. We also found that the synthesis of other anti-oxidant proteins such as thioredoxin-1, glutathione peroxidase, peroxiredoxin 1 and catalase were suppressed by TDI. Furthermore, TDI suppressed nuclear translocation of Nrf2 through suppressing the phosphorylation of mitogen-activated protein kinases (MAPKs); extracellular-regulated kinase ...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3371222</comments>
            <pubDate>Tue, 16 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3371222</guid>        </item>
        <item>
            <title>Rearing environment affects development of the immune system in neonates</title>
            <link>http://www.medworm.com/index.php?rid=3295320&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2010.04090.x</link>
            <description>Early-life exposure to appropriate microbial flora drives expansion and development of an efficient immune system. Aberrant development results in increased likelihood of allergic disease or increased susceptibility to infection. Thus, factors affecting microbial colonization may also affect the direction of immune responses in later life. There is a need for a manipulable animal model of environmental influences on the development of microbiota and the immune system during early life. We assessed the effects of rearing under low- (farm, sow) and high-hygiene (isolator, milk formula) conditions on intestinal microbiota and immune development in neonatal piglets, because they can be removed from the mother in the first 24 h for rearing under controlled conditions and, due to placental struc...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3295320</comments>
            <pubDate>Tue, 23 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3295320</guid>        </item>
        <item>
            <title>Antigen-dependent immunotherapy of non-obese diabetic mice with immature dendritic cells</title>
            <link>http://www.medworm.com/index.php?rid=3284917&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2010.04104.x</link>
            <description>Immunotherapy can be used to induce immunological tolerance by a number of different protocols. During the last decade the ability to use tolerogenic dendritic cells (DCs) to prevent autoimmunity has received much attention. Many studies have attempted to use immature or semi-mature DCs to induce tolerance in the non-obese diabetic (NOD) mouse model of human type 1 diabetes. However, most studies to date have used protocols in which generation of DCs involved a culture step in fetal bovine serum (FBS)-supplemented medium which may affect tolerance induction in a non-specific fashion. Indeed, several studies have shown that DCs cultured in the presence of FBS will induce a powerful T helper type 2 (Th2) immune response towards FBS-related antigens which can suppress an ongoing immune respon...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3284917</comments>
            <pubDate>Fri, 19 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3284917</guid>        </item>
        <item>
            <title>Long-chain polyunsaturated fatty acids are consumed during allergic inflammation and affect T helper type 1 (Th1)- and Th2-mediated hypersensitivity differently</title>
            <link>http://www.medworm.com/index.php?rid=3260092&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2010.04107.x</link>
            <description>This study investigated whether fish (n-3) or sunflower (n-6) oil supplementation affected T helper type 1 (Th1)- and Th2-mediated hypersensitivity in the skin and airways, respectively, and whether the fatty acid serum profile changed during the inflammatory response. Mice were fed regular chow, chow + 10% fish oil or chow + 10% sunflower oil. Mice were immunized with ovalbumin (OVA) resolved in Th1 or Th2 adjuvant. For Th1 hypersensitivity, mice were challenged with OVA in the footpad. Footpad swelling, OVA-induced lymphocyte proliferation and cytokine production in the draining lymph node were evaluated. In the airway hypersensitivity model (Th2), mice were challenged intranasally with OVA and the resulting serum immunoglobulin (Ig)E and eosinophilic lung infiltration were measured. In ...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3260092</comments>
            <pubDate>Thu, 11 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3260092</guid>        </item>
        <item>
            <title>CCR6 identifies lymphoid tissue inducer cells within cryptopatches</title>
            <link>http://www.medworm.com/index.php?rid=3260095&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2010.04103.x</link>
            <description>In this report, we show that lin- c-kit+ lymphocytes express a variety of different chemokine receptors and that CCR6 identifies those cells located within CP. In contrast, cells found outside CP are positive for CXCR3 and exhibit a different surface marker profile, suggesting that at least two different populations of lin- c-kit+ cells are present. The presence of CCR6 does not influence the expression of Notch molecules on lin- c-kit+ cells, nor does it influence Notch ligand expression on bone marrow-derived dendritic cells. In the human gut, CCR6 identifies clusters of lymphocytes resembling murine CP. CCR6 seems to have an important role for lin- c-kit+ cells inside CP, is expressed in a regulated manner and identifies potential human CP. (Source: Clinical and Experimental Immunology)</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3260095</comments>
            <pubDate>Wed, 10 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3260095</guid>        </item>
        <item>
            <title>Interleukin-10 inhibits Mycobacterium bovis bacillus Calmette&amp;#x2013;Gu&amp;eacute;rin (BCG)-induced macrophage cytotoxicity against bladder cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=3260094&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2010.04105.x</link>
            <description>This study was to determine whether interleukin (IL)-10 produced by macrophages in response to BCG is a causative factor for the reduced cytotoxicity in BCG-stimulated C57BL/6 macrophages. Thioglycollate-elicited peritoneal macrophages were prepared and analysed for the BCG induction of cytotoxicity, cytokines and nitric oxide (NO) in vitro. Compared to BCG-stimulated C3H/HeN macrophages, BCG-stimulated C57BL/6 macrophages exhibited reduced killing of bladder cancer MBT-2 cells and MB49 cells. Studies demonstrated further that BCG-stimulated C57BL/6 macrophages produced a high level of IL-10, which correlated with reduced production of tumour necrosis factor (TNF)-[alpha], IL-6 and NO. Neutralizing endogenous IL-10 during BCG stimulation increased C57BL/6 macrophage cytotoxicity against MB...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3260094</comments>
            <pubDate>Wed, 10 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3260094</guid>        </item>
        <item>
            <title>Infant CD4 C868T polymorphism is associated with increased human immunodeficiency virus (HIV-1) acquisition</title>
            <link>http://www.medworm.com/index.php?rid=3236901&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2010.04096.x</link>
            <description>The C868T single nucleotide polymorphism (SNP) in the CD4 receptor encodes an amino acid change that could alter its structure and influence human immunodeficiency virus (HIV-1) infection risk. HIV-1-infected pregnant women in Nairobi were followed with their infants for 1 year postpartum. Among 131 infants, those with the 868T allele were more likely than wild-type infants to acquire HIV-1 overall [hazard ratio (HR) = 1·92, 95% confidence interval (CI) 1·05, 3·50, P = 0·03; adjusted HR = 2·03, 95% CI 1·03, 3·98, P = 0·04], after adjusting for maternal viral load. This SNP (an allele frequency of [sim]15% in our cohort) was associated with increased susceptibility to mother-to-child HIV-1 transmission, consistent with a previous study on this polymorphism among Nairobi sex workers....</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3236901</comments>
            <pubDate>Thu, 04 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3236901</guid>        </item>
        <item>
            <title>Schistosoma mansoni antigens modulate the allergic response in a murine model of ovalbumin-induced airway inflammation</title>
            <link>http://www.medworm.com/index.php?rid=3236903&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04084.x</link>
            <description>Schistosoma mansoni infection has been associated with protection against allergies. The mechanisms underlying this association may involve regulatory cells and cytokines. We evaluated the immune response induced by the S. mansoni antigens Sm22·6, PIII and Sm29 in a murine model of ovalbumin (OVA)-induced airway inflammation. BALB/c mice were sensitized with subcutaneously injected OVA-alum and challenged with aerolized OVA. Mice were given three doses of the different S. mansoni antigens. Lung histopathology, cellularity of bronchoalveolar lavage (BAL) and eosinophil peroxidase activity in lung were evaluated. Immunoglobulin (Ig)E levels in serum and cytokines in BAL were also measured. Additionally, we evaluated the frequency of CD4+forkhead box P3 (FoxP3)+ T cells in cultures stimulate...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3236903</comments>
            <pubDate>Tue, 02 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3236903</guid>        </item>
        <item>
            <title>Interleukin-2 inhibits polarization to T helper type 1 cells and prevents mouse acute graft-versus-host disease through up-regulating suppressors of cytokine signalling-3 expression of naive CD4+ T cells</title>
            <link>http://www.medworm.com/index.php?rid=3236902&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2010.04089.x</link>
            <description>In this study, we found that interleukin (IL)-2 pre-incubation of C57BL/6 naive CD4+ T cells could up-regulate the expression of SOCS-3. Naive CD4+ T cells constitutively expressed low levels of SOCS-3 mRNA. SOCS-3 mRNA began to rise after 4 h, and reached peak level at 6 h. At 8 h it began to decrease. High expression of SOCS-3 mRNA induced by IL-2 could inhibit the proliferation of naive CD4+ T cells following stimulation with allogeneic antigen. IL-2-induced high SOCS-3 expression in naive CD4+ T cells could inhibit polarization to Th1 with stimulation of allogeneic antigens. We have demonstrated that IL-2-induced high SOCS-3 expression in naive CD4+ T cells could reduce the incidence of aGVHD between major histocompatibility complex (MHC) completely mismatched donor and host when high ...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3236902</comments>
            <pubDate>Tue, 02 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3236902</guid>        </item>
        <item>
            <title>Modulation of immune responses through direct activation of Toll-like receptors to T cells</title>
            <link>http://www.medworm.com/index.php?rid=3221499&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2010.04091.x</link>
            <description>Toll-like receptors (TLRs), which are a family of pattern recognition receptors (PRRs), are involved critically in the generation and regulation of innate immunity as well as initiation of subsequent adaptive immune responses. However, recent research results showed that different subsets of T cells express certain types of TLRs during development and activation stages. Importantly, TLRs participate in the direct regulation of adaptive immune response, possibly as co-stimulatory molecules. In this review we summarize recent studies about the novel regulation of TLRs on the homeostasis and immunity of different T cell subtypes including CD4+CD25+T regulatory cells (Treg) and interleukin (IL)-17-producing CD4+T cells (T helper type 17). The direct involvement of TLRs in T cell-mediated immun...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3221499</comments>
            <pubDate>Sat, 30 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3221499</guid>        </item>
        <item>
            <title>Impaired host defence against Mycobacterium avium in mice with chronic granulomatous disease</title>
            <link>http://www.medworm.com/index.php?rid=3182782&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2010.04092.x</link>
            <description>Patients with chronic granulomatous disease (CGD), an inherited disorder of phagocytic cells, often contract recurrent life-threatening bacterial and fungal infections. CGD is considered to arise from a functional defect of the O2-generating nicotinamide adenine dinucleotide phosphate (NADPH) oxidase in phagocytes. To determine whether or not NADPH oxidase is crucial to the host defence against Mycobacterium avium, we investigated the response against M. avium using CGD model mice (gp91-phox-) of C57BL/6 strain. A tracheal injection of 1 × 107 colony-forming units (CFU)/head of M. avium strain FN into the CGD mice resulted in a pulmonary infection, while also increasing the mortality rate. In contrast, normal C57BL/6 mice injected with same dose of the organisms did not develop severe pul...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3182782</comments>
            <pubDate>Tue, 19 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3182782</guid>        </item>
        <item>
            <title>The increased mucosal mRNA expressions of complement C3 and interleukin-17 in inflammatory bowel disease</title>
            <link>http://www.medworm.com/index.php?rid=3182781&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2010.04093.x</link>
            <description>Recent studies have demonstrated that the complement system participates in the regulation of T cell functions. To address the local biosynthesis of complement components in inflammatory bowel disease (IBD) mucosa, we investigated C3 and interleukin (IL)-17 mRNA expression in mucosal samples obtained from patients with IBD. The molecular mechanisms underlying C3 induction were investigated in human colonic subepithelial myofibroblasts (SEMFs). IL-17 and C3 mRNA expressions in the IBD mucosa were evaluated by real-time polymerase chain reaction. The C3 levels in the supernatant were determined by enzyme-linked immunosorbent assay. IL-17 and C3 mRNA expressions were elevated significantly in the active lesions from ulcerative colitis (UC) and Crohn's disease (CD) patients. There was a signif...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3182781</comments>
            <pubDate>Tue, 19 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3182781</guid>        </item>
        <item>
            <title>Inhibition of transforming growth factor-&amp;#x03B2; signalling attenuates interleukin (IL)-18 plus IL-2-induced interstitial lung disease in mice</title>
            <link>http://www.medworm.com/index.php?rid=3182780&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2010.04094.x</link>
            <description>In this study, we investigated the role of transforming growth factor (TGF)-[beta] signalling in the pathogenesis of ILD by using model mice. Injection of interleukin (IL)-18 plus IL-2 in C57BL6 (B6) mice resulted in acute ILD by infiltration of natural killer (NK) cells and a significant increase of TGF-[beta] mRNA in the lung. To examine the pathogenetic role of TGF-[beta] in ILD mice, we used SB-431542 (4-[4-(1,3-benzodioxol-5-yl)-5-(2-pyridinyl)-1H-imidazol-2-yl]-benzamide), which is a potent and selective inhibitor of TGF-[beta] receptor I (T[beta]RI), also known as activin receptor-like kinase 5 (ALK5). Treatment of B6-ILD mice with SB-431542 resulted in improvement of ILD, delay in mortality, reduction of the expression of interferon (IFN)-[gamma] and IL-6 in the lungs. The same tre...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3182780</comments>
            <pubDate>Tue, 19 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3182780</guid>        </item>
        <item>
            <title>Killer cell immunoglobulin-like receptor (KIR) genes in systemic sclerosis</title>
            <link>http://www.medworm.com/index.php?rid=3176873&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2010.04095.x</link>
            <description>A previous study has suggested that the combination KIR2DS2+/KIR2DL2- was related to increased risk for systemic sclerosis (SSc), while others have failed to reproduce this finding. Our objective was to study this matter further and test the association of other KIR genes with SSc. One hundred and ten SSc patients and 115 healthy bone marrow donors were enrolled in a case[ndash]control study. Blood was collected for DNA extraction; typing of 15 KIR genes and human leucocyte antigen-C (HLA-C) was made by polymerase chain reaction with sequence specific primers (PCR[ndash]SSP), followed by electrophoresis on agarose gel. Patients underwent clinical evaluation, serology, Doppler echocardiography and chest high-resolution computed tomography. The frequency of the inhibitory KIR2DL2 was signifi...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3176873</comments>
            <pubDate>Sat, 16 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3176873</guid>        </item>
        <item>
            <title>An approach to the diagnosis and management of systemic vasculitis revised version with tracked changes removed</title>
            <link>http://www.medworm.com/index.php?rid=3164879&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04078.x</link>
            <description>The systemic vasculitides are a complex and often serious group of disorders which, while uncommon, require careful management in order to ensure optimal outcome. In most cases there is no known cause. Multi-system disease is likely to be fatal without judicious use of immunosuppression. A prompt diagnosis is necessary to preserve organ function. Comprehensive and repeated disease assessment is a necessary basis for planning therapy and modification of treatment protocols according to response. Therapies typically include glucocorticoids and, especially for small and medium vessel vasculitis, an effective immunosuppressive agent. Cyclophosphamide is currently the standard therapy for small vessel multi-system vasculitis, but other agents are now being evaluated in large randomized trials. ...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3164879</comments>
            <pubDate>Wed, 13 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3164879</guid>        </item>
        <item>
            <title>Epitope shift of proteinase-3 anti-neutrophil cytoplasmic antibodies in patients with small vessel vasculitis</title>
            <link>http://www.medworm.com/index.php?rid=3143494&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04063.x</link>
            <description>Anti-neutrophil cytoplasmic antibodies against proteinase 3 (PR3-ANCA) are used as diagnostic tools for patients with small vessel vasculitis (AASV). We have produced chimeric mouse/human PR3 molecules and investigate changes in reactivity over time and the possible relationship between epitope specificity and clinical course. Thirty-eight PR3-ANCA-positive patients diagnosed between 1990 and 2003 were followed until December 2005. Plasma was collected at each out-patient visit and older samples were retrieved retrospectively. Patients reacted with multiple epitopes at the time of diagnosis. At subsequent relapses 12 patients shifted reactivity, in 11 cases from epitopes located in the C-terminal towards epitopes in the N-terminal. Patients with reactivity against N-terminal parts of PR3 a...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3143494</comments>
            <pubDate>Wed, 06 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3143494</guid>        </item>
        <item>
            <title>Caffeic acid phenethyl ester inhibits nuclear factor-&amp;#x03BA;B and protein kinase B signalling pathways and induces caspase-3 expression in primary human CD4+ T cells</title>
            <link>http://www.medworm.com/index.php?rid=3143493&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04067.x</link>
            <description>This study provides a new insight into the mechanisms of CAPE for immune regulation and a rationale for the use of propolis for the treatment of allergic disorders. (Source: Clinical and Experimental Immunology)</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3143493</comments>
            <pubDate>Wed, 06 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3143493</guid>        </item>
        <item>
            <title>High-density lipoprotein affects antigen presentation by interfering with lipid raft: a promising anti-atherogenic strategy</title>
            <link>http://www.medworm.com/index.php?rid=3143492&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04068.x</link>
            <description>Atherosclerosis is a chronic inflammatory disease. Immunomodulation of atherosclerosis emerges as a promising approach to prevention and treatment of this widely prevalent disease. The function of high-density lipoprotein (HDL) to promote reverse cholesterol transport may explain the ability of its protection against atherosclerosis. Findings that HDL and apolipoprotein A-I (apoA-I) inhibited the ability of antigen presenting cells (APCs) to stimulate T cells might be attributed to lipid raft, a cholesterol-rich microdomain exhibiting functional properties depending largely upon its lipid composition. Thus, modulating cholesterol in lipid raft may provide a promising anti-atherogenic strategy. (Source: Clinical and Experimental Immunology)</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3143492</comments>
            <pubDate>Wed, 06 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3143492</guid>        </item>
        <item>
            <title>Sequential expression of macrophage anti-microbial/inflammatory and wound healing markers following innate, alternative and classical activation</title>
            <link>http://www.medworm.com/index.php?rid=3143496&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04086.x</link>
            <description>The present study examines the temporal dynamics of macrophage activation marker expression in response to variations in stimulation. We demonstrate that markers can be categorized as 'early' (expressed most abundantly at 6 h post-stimulation) or 'late' (expressed at 24 h post-stimulation). Thus nos2 and p40 (IL-12/IL-23) are early markers of innate and classical activation, while dectin-1 and mrc-1 are early markers and fizz1 (found in inflammatory zone-1) and ym1 are late markers of alternative activation. Furthermore, argI is a late marker of both innate and alternative activation. The ability of interferon (IFN)-[gamma] to alter these activation markers was studied at both the protein level and gene level. As reported previously, IFN-[gamma] was able to drive macrophages towards the cl...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3143496</comments>
            <pubDate>Tue, 05 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3143496</guid>        </item>
        <item>
            <title>Islet inflammation and CXCL10 in recent-onset type 1 diabetes</title>
            <link>http://www.medworm.com/index.php?rid=3143495&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04087.x</link>
            <description>Type 1 diabetes results from a T cell-mediated destruction of insulin-producing pancreatic [beta] cells. Little is known on local factors contributing to migration of T cells to pancreatic tissue. We recently demonstrated evidence of viral infection in [beta] cells in several recent-onset type 1 diabetes patients. Islet inflammation was analysed in a series of new- or recent-onset type 1 diabetic patients and non-diabetic control subjects. Autoimmune T cell reactivity was studied in lymphocytes derived from pancreas-draining lymph nodes of one recent-onset type 1 diabetes patient in partial clinical remission. Insulitic lesions were characterized by presence of [beta] cells, elevated levels of the chemokine CXCL10 and infiltration of lymphocytes expressing the corresponding chemokine recep...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3143495</comments>
            <pubDate>Tue, 05 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3143495</guid>        </item>
        <item>
            <title>High density of intraepithelial &amp;#x03B3;&amp;#x03B4; lymphocytes and deposits of immunoglobulin (Ig)M anti-tissue transglutaminase antibodies in the jejunum of coeliac patients with IgA deficiency</title>
            <link>http://www.medworm.com/index.php?rid=3107250&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04077.x</link>
            <description>The diagnosis of coeliac disease (CD) represents a special challenge in selective immunoglobulin (Ig)A deficiency (IgAD). A high density of T cell receptor (TCR)[gamma][delta]+ intraepithelial lymphocytes (IELs) and intestinal IgA anti-tissue transglutaminase 2 (anti-TG2) antibody deposits are suggestive of CD. We analysed the density of TCR[gamma][delta]+ IELs and the deposition of IgM anti-TG2 antibodies in the jejunal mucosa of IgAD patients with and without CD. Immunohistochemical analyses for the number of CD3+ and TCR[gamma][delta]+ IELs and double immunofluorescence assay for IgM anti-TG2 antibody deposits were performed in biopsies from 25 children with IgAD (nine untreated CD, seven potential CD and nine without CD). Sixteen immunologically intact children without CD represented t...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3107250</comments>
            <pubDate>Mon, 21 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3107250</guid>        </item>
        <item>
            <title>Calreticulin is a B cell molecular target in some gastrointestinal malignancies</title>
            <link>http://www.medworm.com/index.php?rid=3097486&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04085.x</link>
            <description>Calreticulin, upon translocation to the cell surface, plays a critical role in the recognition of tumour cells and in experimentally induced cellular anti-tumour immunity. However, less is known about anti-calreticulin antibodies and their role in malignancies. Using enzyme-linked immunosorbent assay (ELISA), we found immunoglobulin (Ig)A and/or IgG anti-calreticulin antibodies in sera of approximately 63% of patients with hepatocellular carcinoma (HCC), 57% of patients with colorectal adenocarcinoma (CRA) and 47% of patients with pancreatic adenocarcinoma (PACA), while healthy controls, patients with viral hepatitis C and with chronic pancreatitis reached only 2%, 20% and 31% seropositivity, respectively. We found significantly elevated mean levels of IgA anti-calreticulin antibodies (P &lt;...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3097486</comments>
            <pubDate>Fri, 18 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3097486</guid>        </item>
        <item>
            <title>Immune response to Plasmodium vivax has a potential to reduce malaria severity</title>
            <link>http://www.medworm.com/index.php?rid=3097490&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04075.x</link>
            <description>Plasmodium falciparum infection causes transient immunosuppression during the parasitaemic stage. However, the immune response during simultaneous infections with both P. vivax and P. falciparum has been investigated rarely. In particular, it is not clear whether the host's immune response to malaria will be different when infected with a single or mixed malaria species. Phenotypes of T cells from mixed P. vivax[ndash]P. falciparum (PV-PF) infection were characterized by flow cytometry, and anti-malarial antibodies in the plasma were determined by an enzyme-linked immunosorbent assay. We found the percentage of CD3+[delta]2+-T cell receptor (TCR) T cells in the acute-mixed PV-PF infection and single P. vivax infection three times higher than in the single P. falciparum infection. This impl...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3097490</comments>
            <pubDate>Thu, 17 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3097490</guid>        </item>
        <item>
            <title>T cell activation profiles in different granulomatous interstitial lung diseases&amp;nbsp;&amp;#x2013;&amp;nbsp;a role for CD8+CD28null cells?</title>
            <link>http://www.medworm.com/index.php?rid=3097489&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04076.x</link>
            <description>Lymphocytes play a crucial role in lung inflammation. Different interstitial lung diseases may show distinct lymphocyte activation profiles. The aim of this study was to examine the expression of a variety of activation markers on T lymphocyte subsets from blood and bronchoalveolar lavage fluid (BALF) of patients with different granulomatous interstitial lung diseases and healthy controls. Bronchoalveolar lavage cells and blood cells from 23 sarcoidosis patients, seven patients with hypersensitivity pneumonitis and 24 healthy controls were analysed. Lymphocyte activation status was determined by flow cytometry. Lymphocytes were stained with antibodies against CD3, CD4, CD8, CD25, CD28, CD69, very late antigen-1 (VLA)-1, VLA-4 and human leucocyte antigen D-related (HLA-DR). In general, CD28...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3097489</comments>
            <pubDate>Thu, 17 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3097489</guid>        </item>
        <item>
            <title>Dendritic cells pulsed with antigen-specific apoptotic bodies prevent experimental type 1 diabetes</title>
            <link>http://www.medworm.com/index.php?rid=3097488&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04082.x</link>
            <description>Dendritic cells (DCs) are powerful antigen-presenting cells capable of maintaining peripheral tolerance. The possibility to generate tolerogenic DCs opens new therapeutic approaches in the prevention or remission of autoimmunity. There is currently no treatment inducing long-term tolerance and remission in type 1 diabetes (T1D), a disease caused by autoimmunity towards [beta] cells. An ideal immunotherapy should inhibit the autoimmune attack, avoid systemic side effects and allow islet regeneration. Apoptotic cells [ndash] a source of autoantigens [ndash] are cleared rapidly by macrophages and DCs through an immunologically silent process that contributes to maintaining tolerance. Our aims were to prevent T1D and to evaluate the re-establishment of peripheral tolerance using autologous DCs...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3097488</comments>
            <pubDate>Thu, 17 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3097488</guid>        </item>
        <item>
            <title>Vitamin K3 attenuates lipopolysaccharide-induced acute lung injury through inhibition of nuclear factor-&amp;#x03BA;B activation</title>
            <link>http://www.medworm.com/index.php?rid=3097487&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04083.x</link>
            <description>In this study, we investigated the anti-inflammatory effects of vitamin K3 in in vitro cultured cell experiments and in vivo animal experiments. In human embryonic kidney (HEK)293 cells, vitamin K3 inhibited the tumour necrosis factor (TNF)-[alpha]-evoked translocation of nuclear factor (NF)-[kappa]B into the nucleus, although vitamins K1 and K2 did not. Vitamin K3 also suppressed the lipopolysaccharide (LPS)-induced nuclear translocation of NF-[kappa]B and production of TNF-[alpha] in mouse macrophage RAW264·7 cells. Moreover, the addition of vitamin K3 before and after LPS administration attenuated the severity of lung injury in an animal model of acute lung injury/acute respiratory distress syndrome (ARDS), which occurs in the setting of acute severe illness complicated by systemic inf...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3097487</comments>
            <pubDate>Thu, 17 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3097487</guid>        </item>
        <item>
            <title>The other side of immunoglobulin G: suppressor of inflammation</title>
            <link>http://www.medworm.com/index.php?rid=3093349&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04081.x</link>
            <description>Immunoglobulin G (IgG) molecules can have two completely opposite functions. On one hand, they induce proinflammatory responses and recruit innate immune effector cells during infection with pathogenic microorganisms or autoimmune disease. On the other hand, intravenous infusion of high doses of pooled IgG molecules from thousands of donors [intravenous IG (IVIG) therapy] represents an efficient anti-inflammatory treatment for many autoimmune diseases. Whereas our understanding of the mechanism of the proinflammatory activity of IgG is quite advanced, we are only at the very beginning to comprehend how the anti-inflammatory activity comes about and what cellular and molecular players are involved in this activity. This review will summarize our current knowledge and focus upon the two majo...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3093349</comments>
            <pubDate>Thu, 17 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3093349</guid>        </item>
        <item>
            <title>Economic evaluation of immunoglobulin replacement in patients with primary antibody deficiencies</title>
            <link>http://www.medworm.com/index.php?rid=3093350&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04079.x</link>
            <description>This study aims to determine whether SCIG is cost-effective compared with IVIG from a French social insurance perspective. Because both methods of administration provide similar efficacies, a cost-minimization analysis was performed. First, costs were calculated through a simulation testing different hypothesis on costs drivers. Secondly, costs were estimated on the basis of field data collected by a questionnaire completed by a population of patients suffering from agammaglobulinaemia and hyper-immunoglobulin (Ig)M syndrome. Patients' satisfaction was also documented. Results of the simulation showed that direct medical costs ranged from [euro]19 484 for home-based IVIG to [euro]25 583 for hospital-based IVIG, with home-based SCIG in between at [euro]24 952 per year. Estimations made from...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3093350</comments>
            <pubDate>Wed, 16 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3093350</guid>        </item>
        <item>
            <title>Decreased expression of Fli-1 in bone marrow-derived haematopoietic cells significantly affects disease development in Murphy Roths Large/lymphoproliferation (MRL/lpr) mice</title>
            <link>http://www.medworm.com/index.php?rid=3089988&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04080.x</link>
            <description>In this study, bone marrow (BM) transplantation was used to investigate the role of decreased expression of Fli-1 in haematopoietic versus non-haematopoietic cell lineages in autoimmune disease development. Wild-type (WT) MRL/lpr that received BM from Fli-1+/[minus] MRL/lpr mice had statistically significantly lower autoantibodies, less proteinuria, reduced renal disease and prolonged survival compared to WT MRL/lpr mice that received BM from WT MRL/lpr mice. Although not statistically significant, Fli-1+/[minus] MRL/lpr mice that received BM from WT MRL/lpr mice also had lower autoantibodies and improved survival compared to WT MRL/lpr mice that received BM from WT MRL/lpr mice. Our data indicate that expression of Fli-1 in haematopoietic cell lineages has a significant effect on disease ...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3089988</comments>
            <pubDate>Wed, 16 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3089988</guid>        </item>
        <item>
            <title>Unique activation status of peripheral blood mononuclear cells at acute phase of Kawasaki disease</title>
            <link>http://www.medworm.com/index.php?rid=3089990&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04073.x</link>
            <description>Although Kawasaki disease (KD) is characterized by a marked activation of the immune system with elevations of serum proinflammatory cytokines and chemokines at acute phase, the major sources for these chemical mediators remain controversial. We analysed the activation status of peripheral blood mononuclear cells (PBMCs) by flow cytometry, DNA microarray and quantitative reverse transcription[ndash]polymerase chain reaction. The proportions of CD69+ cells in both natural killer cells and [gamma][delta]T cells at acute-phase KD were significantly higher than those at convalescent-phase KD. Microarray analysis revealed that five genes such as NAIP, IPAF, S100A9, FCGR1A and GCA up-regulated in acute-phase KD and the pathways involved in acute phase KD were related closely to the innate immune...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3089990</comments>
            <pubDate>Tue, 15 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3089990</guid>        </item>
        <item>
            <title>An &amp;#x03B1;-galactosylceramide C20:2 N-acyl variant enhances anti-inflammatory and regulatory T cell-independent responses that prevent type 1 diabetes</title>
            <link>http://www.medworm.com/index.php?rid=3089989&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04074.x</link>
            <description>Protection from type 1 diabetes (T1D), a T helper type 1 (Th1)-mediated disease, is achievable in non-obese diabetic (NOD) mice by treatment with [alpha]-galactosylceramide ([alpha]-GalCer) glycolipids that stimulate CD1d-restricted invariant natural killer T (iNK T) cells. While we have reported previously that the C20:2 N-acyl variant of [alpha]-GalCer elicits a Th2-biased cytokine response and protects NOD mice from T1D more effectively than a form of [alpha]-GalCer that induces mixed Th1 and Th2 responses, it remained to determine whether this protection is accompanied by heightened anti-inflammatory responses. We show that treatment of NOD mice with C20:2 diminished the activation of 'inflammatory' interleukin (IL)-12 producing CD11chighCD8+ myeloid dendritic cells (mDCs) and augmente...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3089989</comments>
            <pubDate>Tue, 15 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3089989</guid>        </item>
        <item>
            <title>Immunological and clinical profile of adult patients with selective immunoglobulin subclass deficiency: response to intravenous immunoglobulin therapy</title>
            <link>http://www.medworm.com/index.php?rid=3083355&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04062.x</link>
            <description>Selective immunoglobulin (Ig)G3 subclass deficiency in adults, especially its immunological profile, has not been described previously in detail. Therefore, a retrospective chart review was conducted to characterize the immune profile and clinical manifestations in adult patients with selective IgG3 deficiency. We reviewed the charts of 17 adult patients attending our subspeciality immunology clinic with a diagnosis of selective IgG3 deficiency. The following immunological test results were recorded: lymphocyte subsets, proliferative response to mitogens (phytohaemagglutinin, concanavalin A, pokeweed mitogen) and soluble antigens (mumps, Candida albicans, tetanus toxoid), specific antibody response to tetanus toxoid and pneumococcal antigens, neutrophil oxidative burst and natural killer c...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3083355</comments>
            <pubDate>Mon, 14 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3083355</guid>        </item>
        <item>
            <title>Low numbers of CD8+ T lymphocytes in hereditary haemochromatosis are explained by a decrease of the most mature CD8+ effector memory T cells</title>
            <link>http://www.medworm.com/index.php?rid=3083354&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04066.x</link>
            <description>Low CD8+ T lymphocyte numbers have long been described in hereditary haemochromatosis (HH). Recently, two conserved haplotypes localized near the microsatellite D6S105 at the major histocompatibility complex (MHC) class I region were described predicting the clinical expression of HH and the CD8+ T lymphocyte numbers. The A-A-T haplotype was associated with a severe clinical expression of HH and low CD8+ T lymphocyte numbers, while the G-G-G haplotype was associated with a milder clinical expression of HH and high CD8+ T lymphocyte numbers. As CD8+ T lymphocytes are a very heterogeneous population, in this study we analysed the CD8+ subpopulations of naive, central memory (TCM) and effector memory (TEM), and further subsets of CD8+ TEM cells in 47 HH patients and 68 controls. In addition, ...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3083354</comments>
            <pubDate>Mon, 14 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3083354</guid>        </item>
        <item>
            <title>Decrease of blood dendritic cells and increase of tissue-infiltrating dendritic cells are involved in the induction of Sj&amp;ouml;gren's syndrome but not in the maintenance</title>
            <link>http://www.medworm.com/index.php?rid=3083353&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04071.x</link>
            <description>We examined 24 secondary SS and 29 primary SS patients. A direct correlation between the decreased number of myeloid DCs and the duration of Sicca syndrome in primary and secondary SS was observed; namely, the reduction of myeloid DCs in blood was restored spontaneously with duration time of Sicca syndrome. We also examined the immunohistochemical staining of salivary glands of SS patients with monoclonal antibodies against fascin, CD11c and human leucocyte antigen DR (HLA-DR). Fascin+ or CD11c+/HLA-DR+ mononuclear cells were present in the salivary glands of secondary SS patients, as in primary SS. However, fascin+ mononuclear cells were barely detected in the salivary glands of a chronic phase of SS patients. We also found a negative correlation between the frequency of blood myeloid DCs...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3083353</comments>
            <pubDate>Mon, 14 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3083353</guid>        </item>
        <item>
            <title>Anti-PR3 immune responses induce segmental and necrotizing glomerulonephritis</title>
            <link>http://www.medworm.com/index.php?rid=3083352&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04072.x</link>
            <description>In this study, we demonstrate that PR3-specific autoimmune responses are pathogenic in non-obese diabetic (NOD) mice with an impaired regulatory arm of the immune response. Immunization of autoimmunity prone NOD mice with rmPR3 (recombinant mouse PR3) in complete Freund's adjuvant (CFA) resulted in high levels of c-ANCA, without detectable disease development. However, when splenocytes from these immunized mice were transferred into immunodeficient NOD[ndash]severe combined immunodeficiency (SCID) mice, the recipient mice developed vasculitis and severe segmental and necrotizing glomerulonephritis. No disease developed in NOD[ndash]SCID mice that received splenocytes from the CFA-alone-immunized donors (controls), indicating that disease development depends upon PR3-specific immune respons...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3083352</comments>
            <pubDate>Mon, 14 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3083352</guid>        </item>
        <item>
            <title>Systemic and local anti-C5 therapy reduces the disease severity in experimental autoimmune uveoretinitis</title>
            <link>http://www.medworm.com/index.php?rid=3057635&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04070.x</link>
            <description>Activation of complement occurs during autoimmune retinal and intraocular inflammatory disease as well as neuroretinal degenerative disorders. The cleavage of C5 into fragments C5a and C5b is a critical event during the complement cascade. C5a is a potent proinflammatory anaphylatoxin capable of inducing cell migration, adhesion and cytokine release, while membrane attack complex C5b-9 causes cell lysis. Therapeutic approaches to prevent complement-induced inflammation include the use of blocking monoclonal antibodies (mAb) to prevent C5 cleavage. In these current experiments, the rat anti-mouse C5 mAb (BB5·1) was utilized to investigate the effects of inhibition of C5 cleavage on disease progression and severity in experimental autoimmune uveoretinitis (EAU), a model of organ-specific au...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057635</comments>
            <pubDate>Sat, 05 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3057635</guid>        </item>
        <item>
            <title>Administration of a probiotic associated with nasal vaccination with inactivated Lactococcus lactis-PppA induces effective protection against pneumoccocal infection in young mice</title>
            <link>http://www.medworm.com/index.php?rid=3057637&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04056.x</link>
            <description>Streptococcus pneumoniae is a serious public health problem, especially in developing countries, where available vaccines are not part of the vaccination calendar. We evaluated different respiratory mucosa immunization protocols that included the nasal administration of Lactococcus lactis-pneumococcal protective protein A (PppA) live, inactivated, and in association with a probiotic (Lc) to young mice. The animals that received Lc by the oral and nasal route presented the highest levels of immunoglobulin (Ig)A and IgG anti-PppA antibodies in bronchoalveolar lavages (BAL) and IgG in serum, which no doubt contributed to the protection against infection. However, only the groups that received the live and inactivated vaccine associated with the oral administration of the probiotic were able t...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057637</comments>
            <pubDate>Fri, 04 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3057637</guid>        </item>
        <item>
            <title>Flk-1+ mesenchymal stem cells aggravate collagen-induced arthritis by up-regulating interleukin-6</title>
            <link>http://www.medworm.com/index.php?rid=3057636&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04069.x</link>
            <description>The immunomodulatory ability of mesenchymal stem cells (MSCs) may be used to develop therapies for autoimmune diseases. Flk-1+ MSCs are a population of MSCs with defined phenotype and their safety has been evaluated in Phase 1 clinical trials. We designed this study to evaluate whether Flk-1+ MSCs conferred a therapeutic effect on collagen-induced arthritis (CIA), an animal model of rheumatic arthritis, and to explore the underlying mechanisms. Flk-1+ MSCs, 1[ndash]2 × 106, were injected into CIA mice on either day 0 or day 21. The clinical course of arthritis was monitored. Serum cytokine profile was determined by cytometric bead array kit or enzyme-linked immunosorbent assay. Flk-1+ MSCs and splenocytes co-culture was conducted to explore the underlying mechanisms. Flk-1+ MSCs did not c...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057636</comments>
            <pubDate>Fri, 04 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3057636</guid>        </item>
        <item>
            <title>The therapeutic potential of the filarial nematode-derived immunodulator, ES-62 in inflammatory disease</title>
            <link>http://www.medworm.com/index.php?rid=3045645&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04064.x</link>
            <description>The dramatic recent rise in the incidence of allergic or autoimmune inflammatory diseases in the West has been proposed to reflect the lack of appropriate priming of the immune response by infectious agents such as parasitic worms during childhood. Consistent with this, there is increasing evidence supporting an inverse relationship between worm infection and T helper type 1/17 (Th1/17)-based inflammatory disorders such as rheumatoid arthritis, inflammatory bowel disease, type 1 diabetes and multiple sclerosis. Perhaps more surprisingly, given that such worms often induce strong Th2-type immune responses, there also appears to be an inverse correlation between parasite load and atopy. These findings therefore suggest that the co-evolution of helminths with hosts, which has resulted in the ...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3045645</comments>
            <pubDate>Wed, 02 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3045645</guid>        </item>
        <item>
            <title>T cell sensitivity and the outcome of viral infection</title>
            <link>http://www.medworm.com/index.php?rid=3045647&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04047.x</link>
            <description>The importance of CD8+ T cells in the control of viral infections is well established. However, what differentiates CD8+ T cell responses in individuals who control infection and those who do not is not well understood. 'Functional sensitivity' describes an important quality of the T cell response and is determined in part by the affinity of the T cell receptor for antigen. A more sensitive T cell response is generally believed to be more efficient and associated with better control of viral infection, yet may also drive viral mutation and immune escape. Various in vitro techniques have been used to measure T cell sensitivity; however, rapid ex vivo analysis of this has been made possible by the application of the 'magic' tetramer technology. Such tools have potentially important applicati...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3045647</comments>
            <pubDate>Tue, 01 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3045647</guid>        </item>
        <item>
            <title>Interferon signature gene expression is correlated with autoantibody profiles in patients with incomplete lupus syndromes</title>
            <link>http://www.medworm.com/index.php?rid=3045646&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04057.x</link>
            <description>Interferon (IFN) signature genes have been shown to be expressed highly in peripheral blood of patients with systemic lupus erythematosus (SLE), especially in the presence of active disease. However, the expression of this gene signature in individuals with incomplete forms of lupus and the pathogenic relationship between IFN signature genes and autoantibody production have not been explored fully. In the present study, we examined the gene expression and autoantibody profiles of patients diagnosed with incomplete lupus erythematosus (ILE) to determine correlations of the gene expression signature with autoantibody production. Gene expression analysis was carried out on the 24K Illumina Human Refseq-8 arrays using blood samples from 84 subjects, including patients with SLE (n = 27) or ILE ...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3045646</comments>
            <pubDate>Tue, 01 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3045646</guid>        </item>
        <item>
            <title>Pharmacogenomics: a new paradigm to personalize treatments in nephrology patients</title>
            <link>http://www.medworm.com/index.php?rid=3019705&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04065.x</link>
            <description>Although notable progress has been made in the therapeutic management of patients with chronic kidney disease in both conservative and renal replacement treatments (dialysis and transplantation), the occurrence of medication-related problems (lack of efficacy, adverse drug reactions) still represents a key clinical issue. Recent evidence suggests that adverse drug reactions are major causes of death and hospital admission in Europe and the United States. The reasons for these conditions are represented by environmental/non-genetic and genetic factors responsible for the great inter-patient variability in drugs metabolism, disposition and therapeutic targets. Over the years several genetic settings have been linked, using pharmacogenetic approaches, to the effects and toxicity of many agent...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3019705</comments>
            <pubDate>Tue, 24 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3019705</guid>        </item>
        <item>
            <title>Variable effects of cyclophosphamide in rodent models of experimental allergic encephalomyelitis</title>
            <link>http://www.medworm.com/index.php?rid=3000971&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04050.x</link>
            <description>In this study, we have evaluated the effects of cyclophosphamide on the development of experimental allergic encephalomyelitis (EAE) in four EAE rodent models: monophasic EAE in Lewis rats, protracted relapsing (PR)-EAE in DA rats, myelin oligodendrocyte protein (MOG)-induced EAE in C57Bl/6 mice and proteolipid protein (PLP)-induced EAE in Swiss/Jackson Laboratory (SJL) mice. Cyclophosphamide, administered either prophylactically or therapeutically, suppressed most strongly the clinical symptoms of PR-EAE in DA rats. Treated rats in this group also exhibited the lowest degree of inflammatory infiltration of the spinal cord, as well as the lowest levels of nuclear factor kappa B, interleukin-12 and interferon-gamma. Cyclophosphamide prophylactically, but not therapeutically, also delayed si...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3000971</comments>
            <pubDate>Wed, 18 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3000971</guid>        </item>
        <item>
            <title>Calcineurin inhibitors affect B cell antibody responses indirectly by interfering with T cell help</title>
            <link>http://www.medworm.com/index.php?rid=3000970&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04051.x</link>
            <description>In general, humoral immune responses depend critically upon T cell help. In transplantation, prevention or treatment of humoral rejection therefore require drugs that ideally inhibit both B cell and T helper cell activity. Here, we studied the effects of commonly used immunosuppressive drugs [tacrolimus, cyclosporin, mycophenolic acid (MPA) and rapamycin] on T cell helper activity and on T cell-dependent B cell responses. T cells were activated polyclonally in the presence of immunosuppressive drugs in order to analyse the effect of these drugs on T cell proliferation, co-stimulatory ligand expression and cytokines. The impact of immunosuppressive drugs on T cell-dependent immunoglobulin production by B cells was addressed in T[ndash]B cell co-cultures. All drugs affected T cell proliferat...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3000970</comments>
            <pubDate>Wed, 18 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3000970</guid>        </item>
        <item>
            <title>Deficiency in activation-induced cytidine deaminase promotes systemic autoimmunity in lpr mice on a C57BL/6 background</title>
            <link>http://www.medworm.com/index.php?rid=3000969&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04058.x</link>
            <description>Activation-induced deaminase (AID) is a prerequisite for immunoglobulin (Ig) class-switch recombination and somatic hypermutation, which is critical for antibody affinity maturation. IgM and IgG autoantibodies are characteristic of the systemic autoimmune disorders such as lupus. However, the relative contributions of hypermutated high-affinity IgG antibodies and germline-encoded IgM antibodies to systemic autoimmunity are not defined fully. The role of AID in autoimmunity is unclear. The current study used AID-deficient mice to investigate the role of AID in the development and pathogenesis of murine lupus. C57BL/6 mice deficient in both Fas and AID were generated. Compared to their AID-competent littermates, AID[minus]/[minus] lymphoproliferative (lpr) mice produced significantly elevate...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3000969</comments>
            <pubDate>Wed, 18 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3000969</guid>        </item>
        <item>
            <title>Autoantibody-mediated regulation of B cell responses by functional anti-CD22 autoantibodies in patients with systemic sclerosis</title>
            <link>http://www.medworm.com/index.php?rid=2996522&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04059.x</link>
            <description>In this study, we examined the presence and functional property of circulating autoantibodies reacting with CD22 in systemic sclerosis. Serum samples from 10 tight skin (TSK/+) mice and 50 SSc patients were assessed for anti-CD22 autoantibodies by enzyme-linked immunosorbent assays using recombinant mouse or human CD22. The association between anti-CD22 antibodies and clinical features was also investigated in SSc patients. Furthermore, the influence of SSc serum including anti-CD22 autoantibodies for CD22 tyrosine phosphorylation was examined by Western blotting using phosphotyrosine-specific antibodies reacting with four major tyrosine motifs of CD22 cytoplasmic domain. Anti-CD22 autoantibodies were positive in 80% of TSK/+ mice and in 22% of SSc patients. Patients positive for anti-CD22...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2996522</comments>
            <pubDate>Tue, 17 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2996522</guid>        </item>
        <item>
            <title>Anti-transglutaminase antibodies in non-coeliac children suffering from infectious diseases</title>
            <link>http://www.medworm.com/index.php?rid=2985992&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04054.x</link>
            <description>Anti-transglutaminase antibodies are the diagnostic markers of coeliac disease. A role is suggested for infectious agents in the production of anti-transglutaminase antibodies. The aim was to measure positive anti-transglutaminase antibody levels in children with infectious diseases and to compare immunological and biological characteristics of the anti-transglutaminase antibodies derived from these children with that from coeliac patients. Two hundred and twenty-two children suffering from infectious diseases were enrolled prospectively along with seven biopsy-proven coeliacs. Serum samples were tested for anti-transglutaminase antibodies and anti-endomysium antibodies; positive samples were tested for coeliac-related human leucocyte antigen (HLA)-DQ2/8 and anti-viral antibodies. Purified...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2985992</comments>
            <pubDate>Fri, 13 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2985992</guid>        </item>
        <item>
            <title>A review on the vascular features of the hyperimmunoglobulin E syndrome</title>
            <link>http://www.medworm.com/index.php?rid=2985995&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04044.x</link>
            <description>The objective of this review is to characterize the nature and spectrum of vascular abnormalities in HIES patients. Vascular abnormalities in HIES patients were reviewed with Medline and Google Scholar-based searches. In brief, the searches combined terms related to HIES with the terms related to vasculature. Furthermore, reference lists from the original studies and review papers identified were screened. There were vascular abnormalities in 25 patients with HIES. These abnormalities were identified as aneurysms (coronary, aortic, carotid and cerebral), pseudoaneurysms, congenital patent ductus venosus, superior vena cava syndrome, vasculitides, vascular ectasia, thrombosis and others. They may be congenital or acquired, in the veins and arteries, affecting both sexes. These abnormalities...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2985995</comments>
            <pubDate>Thu, 12 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2985995</guid>        </item>
        <item>
            <title>A20 is an early responding negative regulator of Toll-like receptor 5 signalling in intestinal epithelial cells during inflammation</title>
            <link>http://www.medworm.com/index.php?rid=2985994&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04048.x</link>
            <description>Several negative regulatory mechanisms control Toll-like receptor (TLR)-mediated inflammatory responses and restore immune system balance, including the zinc-finger protein A20, a negative regulator of TLR signalling that inhibits nuclear factor kappa B (NF-[kappa]B) activity. In the present study, we investigated TLR-5-mediated A20 expression and its role in intestinal epithelial cells (IECs) during inflammation. HCT-15 and HT-29 cells were stimulated with flagellin, then the expressions of A20, interleukin-1 receptor-associated kinase (IRAK-M) and Tollip were evaluated using RNase protection assay. Furthermore, experimental colitis was induced in tlr4-deficient CH3/HeJ mice by administration of dextran sodium sulphate (DSS), then flagellin was injected anally, and the colonic expression ...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2985994</comments>
            <pubDate>Thu, 12 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2985994</guid>        </item>
        <item>
            <title>Differential effects of glucocorticoids in the establishment and maintenance of endotoxin tolerance</title>
            <link>http://www.medworm.com/index.php?rid=2985993&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04052.x</link>
            <description>In this report we demonstrate, using a mouse model, that while the maintenance of tolerance is dependent upon GC, the establishment of tolerance by LPS could be inhibited by dexamethasone (Dex), a synthetic GC. Conversely, we demonstrated that mifepristone (RU486), a known GC receptor antagonist, was capable of inducing a transient and reversible disruption of endotoxin tolerance, also permitting partial restoration of the humoral immune response in LPS tolerant/immunosuppressed mice. These results are encouraging for the management of immunosuppression in sepsis and/or non-infectious shock, and deserve further investigation in the future. (Source: Clinical and Experimental Immunology)</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2985993</comments>
            <pubDate>Thu, 12 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2985993</guid>        </item>
        <item>
            <title>Gene expression profiles for the human pancreas and purified islets in Type 1 diabetes: new findings at clinical onset and in long-standing diabetes</title>
            <link>http://www.medworm.com/index.php?rid=2982274&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04053.x</link>
            <description>Type 1 diabetes (T1D) is caused by the selective destruction of the insulin-producing [beta] cells of the pancreas by an autoimmune response. Due to ethical and practical difficulties, the features of the destructive process are known from a small number of observations, and transcriptomic data are remarkably missing. Here we report whole genome transcript analysis validated by quantitative reverse transcription[ndash]polymerase chain reaction (qRT[ndash]PCR) and correlated with immunohistological observations for four T1D pancreases (collected 5 days, 9 months, 8 and 10 years after diagnosis) and for purified islets from two of them. Collectively, the expression profile of immune response and inflammatory genes confirmed the current views on the immunopathogenesis of diabetes and showed s...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2982274</comments>
            <pubDate>Thu, 12 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2982274</guid>        </item>
        <item>
            <title>Translational Mini-Review Series on Th17 Cells: Function and regulation of human T helper 17 cells in health and disease</title>
            <link>http://www.medworm.com/index.php?rid=2982280&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04037.x</link>
            <description>T helper (Th) cell have a central role in modulating immune responses. While Th1 and Th2 cells have long been known to regulate cellular and humoral immunity, Th17 cells have been identified only recently as a Th lineage that regulates inflammation via production of distinct cytokines such as interleukin (IL)-17. There is growing evidence that Th17 cells are pathological in many human diseases, leading to intense interest in defining their origins, functions and developing strategies to block their pathological effects. The cytokines that regulate Th17 differentiation have been the focus of much debate, due primarily to inconsistent findings from studies in humans. Evidence from human disease suggests that their in vivo development is driven by specialized antigen-presenting cells. Knowled...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2982280</comments>
            <pubDate>Wed, 11 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2982280</guid>        </item>
        <item>
            <title>Translational Mini-Review Series on Th17 Cells: Induction of interleukin-17 production by regulatory T cells</title>
            <link>http://www.medworm.com/index.php?rid=2982279&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04038.x</link>
            <description>Uncommitted (naive) CD4+ T helper cells (Thp) can be induced to differentiate to specific lineages according to the local cytokine milieu, towards T helper type 1 (Th1), Th2, Th17 and regulatory T cell (Treg) phenotypes in a mutually exclusive manner. Each phenotype is characterized by unique signalling pathways and expression of specific transcription factors, notably T-bet for Th1, GATA-3 for Th2, forkhead box P3 (FoxP3) for Tregs and receptor-related orphan receptor (ROR)[alpha] and ROR[gamma]t for Th17 cells. Tregs and Th17 cells have been demonstrated to arise from common precursors in a reciprocal manner based on exposure to transforming growth factor (TGF)-[beta] or TGF-[beta] plus interleukin (IL)-6 and carry out diametrically opposing functions, namely suppression or propagation o...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2982279</comments>
            <pubDate>Wed, 11 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2982279</guid>        </item>
        <item>
            <title>Translational Mini-Review Series on Th17 Cells: Are T helper 17 cells really pathogenic in autoimmunity?</title>
            <link>http://www.medworm.com/index.php?rid=2982278&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04039.x</link>
            <description>In this review the authors discuss the evidence for T helper type 17 (Th17) cells as pathogenic T cells in autoimmunity. Studies with cytokine-deficient mice or blocking of interleukin (IL)-17, IL-21 and IL-22 have resulted in a conflicting data set. Although in the experimental autoimmune encephalomyelitis model the role of Th17 cells remains a point of debate, this IL-17-producing T cell in experimental arthritis is clearly contributing to inflammation and destruction. (Source: Clinical and Experimental Immunology)</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2982278</comments>
            <pubDate>Wed, 11 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2982278</guid>        </item>
        <item>
            <title>Translational Mini-Review Series on Th17 Cells: CD4+ T helper cells: functional plasticity and differential sensitivity to regulatory T cell-mediated regulation</title>
            <link>http://www.medworm.com/index.php?rid=2982277&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04040.x</link>
            <description>CD4+ T cells display considerable flexibility in their effector functions, allowing them to tackle most effectively the range of pathogenic infections with which we are challenged. The classical T helper (Th) 1 and Th2 subsets have been joined recently by the Th17 lineage. If not controlled, the potent effector functions (chiefly cytokine production) of which these different cells are capable can lead to (sometimes fatal) autoimmune and allergic inflammation. The primary cell population tasked with providing this control appears to be CD4+ regulatory T (Treg) cells expressing the forkhead box P3 (FoxP3) transcription factor. Here we consider the comparative capacity of FoxP3+ Tregs to influence the polarization, expansion and effector function of Th1, Th2 and Th17 cells in vitro and in viv...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2982277</comments>
            <pubDate>Wed, 11 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2982277</guid>        </item>
        <item>
            <title>Translational Mini-Review Series on Th17 Cells: Development of mouse and human T helper 17 cells</title>
            <link>http://www.medworm.com/index.php?rid=2982276&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04041.x</link>
            <description>There has been a considerable amount of interest in the immunological community about new phenotypic subsets of CD4+ T cells, particularly cells that produce the cytokine interleukin (IL)-17 [named T helper type 17 (Th17) cells]. While the initial discovery of Th17 cells and the pathways that controlled their development was in the mouse, recent attention has shifted to the existence of these cells and the relevant upstream cytokine signals in humans. While it is clear that CD4+ T cells producing IL-17 exist in vivo, their relevance to disease pathogenesis is only just being understood. In this paper, we review the data regarding the generation of human Th17 cells in vitro and the evidence that this effector population is important in human disease states. (Source: Clinical and Experimenta...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2982276</comments>
            <pubDate>Wed, 11 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2982276</guid>        </item>
        <item>
            <title>Recipient NOD2/CARD15 status affects cellular infiltrates in human intestinal graft-versus-host disease</title>
            <link>http://www.medworm.com/index.php?rid=2982275&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04049.x</link>
            <description>Nucleotide-binding oligomerization domain 2/caspase recruitment domain 15 (NOD2/CARD15) polymorphisms have been identified as risk factors of both Crohn's disease and graft-versus-host disease (GVHD) following allogeneic stem cell transplantation. However, the role of these receptors of innate immunity in the pathophysiology of gastrointestinal GVHD is still poorly defined. Immunohistological features of intestinal GVHD were analysed in gastrointestinal biopsies from 58 patients obtained at the time of first onset of intestinal symptoms. The observed changes were correlated with concomitant risk factors and the presence of polymorphisms within the pathogen recognition receptor gene NOD2/CARD15. Intestinal GVHD was associated with a stage-dependent decrease in CD4 T cell infiltrates and an ...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2982275</comments>
            <pubDate>Wed, 11 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2982275</guid>        </item>
        <item>
            <title>Toll-like receptor 4 expression is increased in circulating mononuclear cells of patients with immunoglobulin A nephropathy</title>
            <link>http://www.medworm.com/index.php?rid=2964230&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04045.x</link>
            <description>This study shows for the first time an up-regulation of TLR-4 in circulating mononuclear cells of patients with IgAN, particularly in association with proteinuria and heavy microscopic haematuria. (Source: Clinical and Experimental Immunology)</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2964230</comments>
            <pubDate>Fri, 06 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2964230</guid>        </item>
        <item>
            <title>Milder clinical hyperimmunoglobulin E syndrome phenotype is associated with partial interleukin-17 deficiency</title>
            <link>http://www.medworm.com/index.php?rid=2940593&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04043.x</link>
            <description>Mutations in the signal transducer and activator of transcription 3 (STAT3) were reported to cause hyperimmunoglobulin E syndrome (HIES). The present study investigates T helper type 17 (Th17) responses triggered by the relevant stimuli Staphylococcus aureus and Candidia albicans in five 'classical' HIES patients, and a family with three patients who all had a milder HIES phenotype. We demonstrate that patients with various forms of HIES have different defects in their Th17 response to S. aureus and C. albicans, and this is in line with the clinical features of the disease. Interestingly, a partial deficiency of interleukin (IL)-17 production, even when associated with STAT3 mutations, leads to a milder clinical phenotype. We also observed defective Th17 responses in patients with the 'cla...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2940593</comments>
            <pubDate>Fri, 30 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2940593</guid>        </item>
        <item>
            <title>Functional analysis of dendritic cell&amp;#x2013;T cell interaction in sarcoidosis</title>
            <link>http://www.medworm.com/index.php?rid=2940592&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04046.x</link>
            <description>In this study, we investigate the interaction between monocyte-derived dendritic cells and T cells in patients with sarcoidosis compared to normal controls (n = 8 each) by examining the kinetics of autologous and allogeneic mixed leucocyte reactions over 9[ndash]10 days. We found markedly depressed proliferation kinetics in autologous DC-peripheral blood mononuclear cell (PBMC) co-cultures from sarcoid patients compared to normal subjects. In allogeneic experiments PBMCs from patients showed a reduced response to allogeneic DCs from a single donor, but no difference was observed in the ability of patients and control DCs to stimulate proliferation of allogeneic PBMC from a single donor. We conclude that there is a markedly impaired autologous mixed leucocyte reaction (MLR) in sarcoidosis p...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2940592</comments>
            <pubDate>Fri, 30 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2940592</guid>        </item>
        <item>
            <title>Allergic women show reduced T helper type 1 alloresponses to fetal human leucocyte antigen mismatch during pregnancy</title>
            <link>http://www.medworm.com/index.php?rid=2917227&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04042.x</link>
            <description>This study explored the effects of human leucocyte antigen (HLA) mismatch on materno[ndash]fetal interactions detected as cytokine responses and lymphoproliferation in mixed lymphocyte reactions, and whether this was altered in allergic women (n = 62) who have a Th2 propensity compared with non-allergic women (n = 65). HLA-DR[beta]1 mismatch was associated with significantly increased Th1 interferon (IFN)-[gamma], Th2 interleukin (IL)-13 and lymphoproliferative responses by both mothers and fetuses. Allergic women showed significantly lower IFN-[gamma] Th1 production in response to HLA-DR[beta]1 mismatch. The infants of these women also showed significantly lower IL-10 and lower IFN-[gamma] production relative to IL-13. Both HLA-DR[beta]1 mismatch and maternal allergy had significant indep...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2917227</comments>
            <pubDate>Thu, 22 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2917227</guid>        </item>
        <item>
            <title>Complement activation pathways in murine immune complex-induced arthritis and in C3a and C5a generation in vitro</title>
            <link>http://www.medworm.com/index.php?rid=2905759&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04035.x</link>
            <description>The alternative pathway (AP) of complement alone is capable of mediating immune complex-induced arthritis in the collagen antibody-induced arthritis (CAIA) model in mice. Whether the classical pathway (CP) or lectin pathway (LP) alone can mediate CAIA is not known. Using mice genetically deficient in different complement components, our results reported herein establish that the CP and LP alone are each incapable of mediating CAIA. A lower level or absence of C3 and/or C5 activation by the CP may be possible explanations for the importance of the AP in CAIA and in many murine models of disease. In addition, other investigators have reported that CP C5 convertase activity is absent in mouse sera. To address these questions, we employed an in vitro system of adherent immunoglobulin (Ig)G-ind...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2905759</comments>
            <pubDate>Mon, 19 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2905759</guid>        </item>
        <item>
            <title>Activation profile of Toll-like receptors of peripheral blood lymphocytes in patients with systemic lupus erythematosus</title>
            <link>http://www.medworm.com/index.php?rid=2900018&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04036.x</link>
            <description>Systemic lupus erythematosus (SLE) is a systemic autoimmune disease associated with aberrant activation of T and B lymphocytes for the production of inflammatory cytokines and autoreactive antibodies. Animal studies of SLE have indicated that Toll-like receptors (TLR) are important in the pathogenesis of murine lupus. In the present clinical study, differential protein expressions of TLR-1[ndash]9 of monocytes and different lymphocyte subsets from patients with SLE and normal control subjects were determined by flow cytometry. Results showed that the expression of intracellular TLRs (TLR-3, -8, -9) and extracellular TLRs (TLR-1, -2, -4, -5, -6) were elevated in monocytes, CD4+ T lymphocytes, CD8+ T lymphocytes and B lymphocytes of SLE patients compared to control subjects (all P &lt; 0·001)....</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2900018</comments>
            <pubDate>Fri, 16 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2900018</guid>        </item>
        <item>
            <title>Depletion of CD4+CD25+ regulatory T cells enhances natural killer T cell-mediated anti-tumour immunity in a murine mammary breast cancer model</title>
            <link>http://www.medworm.com/index.php?rid=2877346&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04018.x</link>
            <description>In this study, we have shown that Tregs regulate NK T cell function negatively in vitro, suggesting a direct interaction between these cell types. In a murine mammary tumour model, we demonstrated that administration of either [alpha]-GalCer or anti-CD25 antibody alone markedly suppressed tumour formation and pulmonary metastasis, and resulted in an increase in the survival rate up to 44% (from a baseline of 0%). When treatments were combined, depletion of Tregs boosted the anti-tumour effect of [alpha]-GalCer, and the survival rate jumped to 85%. Our results imply a potential application of combining Treg cell depletion with [alpha]-GalCer to stimulate NK T cells for cancer therapy. (Source: Clinical and Experimental Immunology)</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2877346</comments>
            <pubDate>Fri, 09 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2877346</guid>        </item>
        <item>
            <title>Laser microdissection-based analysis of cytokine balance in the kidneys of patients with lupus nephritis</title>
            <link>http://www.medworm.com/index.php?rid=2866408&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04031.x</link>
            <description>To determine the cytokine balance in patients with lupus nephritis (LN), we analysed kidney-infiltrating T cells. Renal biopsy samples from 15 systemic lupus erythematosus (SLE) patients were used. In accordance with the classification of International Society of Nephrology/Renal Pathology Society, they were categorized into Class III, Class III+V (Class III-predominant group, n = 4), Class IV, Class IV+V (Class IV-predominant group, n = 7) and Class V (n = 4) groups. The single-cell samples of both the glomelular and interstitial infiltrating cells were captured by laser-microdissection. The glomerular and interstitial infiltrating T cells produced interleukin (IL)-2, IL-4, IL-10, IL-13 and IL-17 cytokines in the Class III-predominant, Class IV-predominant and Class V groups. Interferon-g...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2866408</comments>
            <pubDate>Tue, 06 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2866408</guid>        </item>
        <item>
            <title>Association of the &amp;#x2212;31C/T functional polymorphism in the interleukin-1&amp;#x03B2; gene with the intractability of Graves' disease and the proportion of T helper type 17 cells</title>
            <link>http://www.medworm.com/index.php?rid=2847832&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04034.x</link>
            <description>In conclusion, our data indicated that the T allele of [minus]31C/T polymorphism in the IL1B gene was involved in the intractability of GD, and this involvement may arise through the differentiation and proliferation of Th17 cells. (Source: Clinical and Experimental Immunology)</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2847832</comments>
            <pubDate>Wed, 30 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2847832</guid>        </item>
        <item>
            <title>16&amp;#x03B1;-Bromoepiandrosterone (HE2000) limits non-productive inflammation and stimulates immunity in lungs</title>
            <link>http://www.medworm.com/index.php?rid=2847834&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04032.x</link>
            <description>16[alpha]-Bromoepiandrosterone (HE2000) is a synthetic steroid that limits non-productive inflammation, enhances protective immunity and improves survival in clinical studies of patients with human immunodeficiency virus (HIV), malaria and tuberculosis infections. We now show that HE2000 decreased nitric oxide production by lipopolysaccharide (LPS)-stimulated RAW264·7 cells. Treatment with HE2000 also reduced non-productive inflammation associated with carrageenan-induced pleurisy and LPS-induced lung injury in mice. In the hapten-carrier reporter antigen popliteal lymph node assay, HE2000 increased absolute numbers of lymphocytes, antigen-presenting cells, hapten-specific immunoglobulin (Ig)M antibody-forming cells and shifted the interferon (IFN)-[gamma]/interleukin (IL)-4 balance towar...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2847834</comments>
            <pubDate>Tue, 29 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2847834</guid>        </item>
        <item>
            <title>Mitogen activated protein kinases: a role in inflammatory bowel disease?</title>
            <link>http://www.medworm.com/index.php?rid=2847833&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04033.x</link>
            <description>Since their discovery more than 15 years ago, the mitogen activated protein kinases (MAPK) have been implicated in an ever-increasingly diverse array of pathways, including inflammatory signalling cascades. Inflammatory bowel diseases (IBD), such as ulcerative colitis and Crohn's disease, are characterized by the perpetual production of inflammatory mediators. Research into the transduction pathway behind this over-production has highlighted the potential mediating role for the MAPKs and their related signalling components. This review highlights some of the research into the role for the MAPKs and their related signalling proteins in influencing the progression of IBD. (Source: Clinical and Experimental Immunology)</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2847833</comments>
            <pubDate>Tue, 29 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2847833</guid>        </item>
        <item>
            <title>Lower numbers of circulating natural killer T (NK T) cells in individuals with human T lymphotropic virus type 1 (HTLV-1) associated neurological disease</title>
            <link>http://www.medworm.com/index.php?rid=2825592&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04019.x</link>
            <description>Human T lymphotropic virus type 1 (HTLV-1) infects 10[ndash]20 million people worldwide. The majority of infected individuals are asymptomatic; however, approximately 3% develop the debilitating neurological disease HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). There is also currently no cure, vaccine or effective therapy for HTLV-1 infection, and the mechanisms for progression to HAM/TSP remain unclear. NK T cells are an immunoregulatory T cell subset whose frequencies and effector functions are associated critically with immunity against infectious diseases. We hypothesized that NK T cells are associated with HAM/TSP progression. We measured NK T cell frequencies and absolute numbers in individuals with HAM/TSP infection from two cohorts on two continents: São Pau...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2825592</comments>
            <pubDate>Wed, 23 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2825592</guid>        </item>
        <item>
            <title>Minimal persistent inflammation in allergic rhinitis: implications for current treatment strategies</title>
            <link>http://www.medworm.com/index.php?rid=2801763&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04017.x</link>
            <description>Patients with allergic rhinitis have traditionally been placed into 'seasonal' and 'perennial' categories, which do not account for the subclinical inflammatory state that exists in many patients. In subjects with seasonal and perennial allergic rhinitis, even subthreshold doses of allergen have been found to cause inflammatory cell infiltration in the nasal mucosa, including increases in expression of cellular adhesion molecules, nasal and conjunctival eosinophilia, and other markers of inflammation, which do not result in overt allergy symptoms. This state [ndash] which has been termed 'minimal persistent inflammation'[ndash] may contribute to hyperreactivity and increased susceptibility to development of clinical symptoms as well as common co-morbidities of allergic rhinitis, such as as...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2801763</comments>
            <pubDate>Wed, 16 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2801763</guid>        </item>
        <item>
            <title>The role of T helper type 17 cells in inflammatory arthritis</title>
            <link>http://www.medworm.com/index.php?rid=2797835&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04016.x</link>
            <description>While T cells have been implicated in the pathogenesis of inflammatory arthritis for more than three decades, the focus on the T helper type 17 (Th17) subset of CD4 T cells and their secreted cytokines, such as interleukin (IL)-17, is much more recent. Proinflammatory actions of IL-17 were first identified in the 1990s, but the delineation of a distinct Th17 subset in late 2005 has sparked great interest in the role of these cells in a broad range of immune-mediated diseases. This review summarizes current understanding of the role of Th17 cells and their products in both animal models of inflammatory arthritis and human immune-driven arthritides. (Source: Clinical and Experimental Immunology)</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2797835</comments>
            <pubDate>Tue, 15 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2797835</guid>        </item>
        <item>
            <title>Calcineurin deficiency decreases inflammatory lesions in transforming growth factor &amp;#x03B2;1-deficient mice</title>
            <link>http://www.medworm.com/index.php?rid=2783186&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04015.x</link>
            <description>Transforming growth factor (TGF) [beta]1) is an immunoregulatory cytokine involved in self-tolerance and lymphocyte homeostasis. Tgfb1 knock-out (KO) mice develop severe multi-focal autoimmune inflammatory lesions due to [Ca2+]i deregulation in T cells, and die within 3 weeks after birth. Because the calcineurin inhibitor FK506 inhibits the hyperresponsiveness of Tgfb1[minus]/[minus] thymocytes, and because calcineurin A[beta] (CNA[beta])-deficient mice do not reject allogenic tumours, we have generated Tgfb1[minus]/[minus]Cnab[minus]/[minus] mice to address whether CNA[beta] deficiency prevents T cell activation and inflammation in Tgfb1[minus]/[minus] mice. Here we show that in Tgfb1[minus]/[minus]Cnab[minus]/[minus] mice inflammation is reduced significantly relative to that in Tgfb1[mi...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2783186</comments>
            <pubDate>Thu, 10 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2783186</guid>        </item>
        <item>
            <title>Increased frequencies of T helper type 17 cells in the peripheral blood of patients with acute myeloid leukaemia</title>
            <link>http://www.medworm.com/index.php?rid=2773161&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04011.x</link>
            <description>In this study, we investigated Th17 cell frequency and secretion of related cytokines in patients with acute myeloid leukaemia (AML). First, we found that Th17 cell frequencies were increased significantly in peripheral blood samples from untreated patients with AML, compared with those from healthy volunteers. Moreover, increased interleukin (IL)-17 concentrations accompanied the increased Th17 cell frequencies in these patients. These results suggest that Th17 cells may play a role in the pathogenesis of AML. Secondly, we found that the increased Th17 cell frequencies were reduced when patients achieved complete remission after chemotherapy, suggesting that measurement of Th17 cell frequencies may have clinical value in the evaluation of therapeutic effect. In addition, we found that IL-...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2773161</comments>
            <pubDate>Mon, 07 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2773161</guid>        </item>
        <item>
            <title>Anti-epidermal growth factor receptor monoclonal antibodies in cancer therapy</title>
            <link>http://www.medworm.com/index.php?rid=2759302&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03992.x</link>
            <description>The epidermal growth factor receptor (EGFR) is a transmembrane tyrosine kinase receptor involved in the proliferation and survival of cancer cells. EGFR is the first molecular target against which monoclonal antibodies (mAb) have been developed for cancer therapy. Here we review the mechanisms underlying the effects of EGFR-specific mAb in cancer therapy. The efficacy of EGFR-specific mAb in cancer occurs thanks to inhibition of EGFR-generated signalling; furthermore, the effects of antibodies on the immune system seem to play an important role in determining the overall anti-tumour response. In this review, attention is focused on cetuximab and panitumumab, two mAb introduced recently into clinical practice for treatment of metastatic colorectal and head and neck cancer which target the e...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2759302</comments>
            <pubDate>Thu, 03 Sep 2009 16:05:04 +0100</pubDate>
            <guid isPermaLink="false">2759302</guid>        </item>
        <item>
            <title>Omega-3 polyunsaturated fatty acids ameliorate the severity of ileitis in the senescence accelerated mice (SAM)P1/Yit mice model</title>
            <link>http://www.medworm.com/index.php?rid=2847836&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04020.x</link>
            <description>Clinical studies using omega-3 polyunsaturated fatty acids ([omega]3-PUFA) to Crohn's disease (CD) are conflicting. Beneficial effects of dietary [omega]3-PUFA intake in various experimental inflammatory bowel disease (IBD) models have been reported. However, animal models of large intestinal inflammation have been used in all previous studies, and the effect of [omega]3 fat in an animal model of small intestinal inflammation has not been reported. We hypothesized that the effects of [omega]3 fat are different between large and small intestine. The aim of this study was to determine whether the direct effect of [omega]3 fat is beneficial for small intestinal inflammation. Senescence accelerated mice (SAM)P1/Yit mice showed remarkable inflammation of the terminal ileum spontaneously. The nu...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2847836</comments>
            <pubDate>Tue, 01 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2847836</guid>        </item>
        <item>
            <title>Alpha versus beta: are we on the way to resolve the mystery as to which is the endogenous ligand for natural killer T cells?</title>
            <link>http://www.medworm.com/index.php?rid=2847835&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04030.x</link>
            <description>Natural killer T (NKT) lymphocytes are a unique subset of cells that play a role in regulating the immune system. For the past decade, studies have focused upon attempts to define these cells and to determine the ligand(s) that are required for their development and peripheral activation. Many research groups have focused upon determining the mechanisms for activating or inhibiting NKT cells in an attempt to control immune-mediated disorders as well as infectious and malignant conditions by using different ligand structures. Alpha-anomeric glycolipids and phospholipids derived from mammalian, bacterial, protozoan and plant species have been suggested as potential ligands for these lymphocytes. Some of these ligands were structured in forms that can bind to CD1d molecules. The lack of alpha...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2847835</comments>
            <pubDate>Tue, 01 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2847835</guid>        </item>
        <item>
            <title>Plasmodium falciparum infection of the placenta impacts on the T helper type 1 (Th1)/Th2 balance of neonatal T cells through CD4+CD25+ forkhead box P3+ regulatory T cells and interleukin-10</title>
            <link>http://www.medworm.com/index.php?rid=2797836&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04014.x</link>
            <description>Placental malaria infection affects the T helper type 1 (Th1)/Th2 balance in neonatal children. We investigated a potential role of regulatory T cells in this balance by comparing T cell responses of cord blood mononuclear cells (CBMC) from parasitized and non-parasitized placenta of Gambian women. CBMC were depleted of CD4+CD25+ forkhead box P3 (FoxP3)+ regulatory T cells and analysed in vitro for their ability to produce interferon (IFN)-[gamma], sCD30 and interleukin (IL)-10 in response to phytohaemagglutinin (PHA), live Plasmodium falciparum, schizont extracts and the recombinant P. falciparum blood stage antigen merozoite surface protein 1 (MSP119). As expected, lower IFN-[gamma] and higher sCD30 responses were observed for the cells from the parasitized group. In addition, higher IL-...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2797836</comments>
            <pubDate>Sun, 16 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2797836</guid>        </item>
        <item>
            <title>Chemokines and common variable immunodeficiency; possible contribution of CCL19, CCL21 and CCR7 to immune dysregulation</title>
            <link>http://www.medworm.com/index.php?rid=2783187&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04013.x</link>
            <description>Common variable immunodeficiency (CVID) is a heterogeneous syndrome characterized by defective immunoglobulin production and high frequency of bacterial infections, autoimmunity and manifestations of chronic inflammation. The homeostatic chemokines CCL19 and CCL21 and their receptor CCR7 are associated with modulation of inflammatory responses. CVID patients have decreased proportions of CCR7+ T cells in peripheral blood and we hypothesized a further dysregulation of CCL19/CCL21/CCR7 in CVID. Serum levels of CCL19 and CCL21 were compared in CVID patients and controls. T cell expression of CCR7 was related to clinical characteristics in CVID patients. Spleens extirpated from CVID patients were analysed for expression of CCL19, CCL21 and CCR7. Peripheral blood mononuclear cells (PBMC) from C...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2783187</comments>
            <pubDate>Tue, 11 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2783187</guid>        </item>
        <item>
            <title>A novel population of human CD56+ human leucocyte antigen D-related (HLA-DR+) colonic lamina propria cells is associated with inflammation in ulcerative colitis</title>
            <link>http://www.medworm.com/index.php?rid=2773169&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04012.x</link>
            <description>Ulcerative colitis (UC) involves inappropriate mucosal immune responses to intestinal microbiota. Gut dendritic cells (DC) are central immunoregulators of the response to commensal bacteria, and the subset of CD11c+ cells within the human leucocyte antigen D-related (HLA-DR+) lineage (lin)[ndash]/dim population are activated in inflammatory bowel disease. We hypothesized that CD11c- cells within this population may also be involved in intestinal inflammation. HLA-DR+ lin[ndash]/dim cells were identified in freshly isolated lamina propria mononuclear cells by multi-colour flow cytometry in 54 UC patients and 22 controls. Proportion and number of CD11c+ and CD11c- cells, and surface expression of activation markers CD40, CD86, Toll-like receptor (TLR)-2, TLR-4, and CD56+[natural killer (NK) ...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2773169</comments>
            <pubDate>Tue, 11 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2773169</guid>        </item>
        <item>
            <title>Reduced incidence and severity of experimental autoimmune arthritis in mice expressing catalytically inactive A disintegrin and metalloproteinase 8 (ADAM8)</title>
            <link>http://www.medworm.com/index.php?rid=2773163&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04009.x</link>
            <description>A disintegrin and metalloproteinase 8 (ADAM8), a catalytically active member of the ADAMs family of enzymes, is expressed primarily on immune cells and thus probably involved in inflammatory responses. ADAM8 is also produced by chondrocytes, and recombinant ADAM8 can induce cartilage catabolism. We therefore decided to test the role of ADAM8 in autoimmune inflammatory arthritis using transgenic mice expressing catalytically inactive ADAM8. Transgenic DBA/1J mice expressing an inactivating point mutation in the ADAM8 gene to change Glu330 to Gln330 (ADAM8EQ) were generated to evaluate the proteolytic function of ADAM8 in an lipopolysaccharide-synchronized collagen-induced arthritis (LPS-CIA) model of autoimmune arthritis. The systemic inflammatory reaction to LPS was also evaluated in these...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2773163</comments>
            <pubDate>Wed, 05 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2773163</guid>        </item>
        <item>
            <title>Mechanisms and clinical implications of glucocorticosteroids in the treatment of allergic rhinitis</title>
            <link>http://www.medworm.com/index.php?rid=2773162&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04010.x</link>
            <description>Allergic rhinitis is a common airway disease characterized by hypersensitivity, exudation, hypersecretion, inflammatory cell infiltration and remodelling. Intranasal glucocorticosteroids are the most effective drugs for controlling the inflammation caused by allergic rhinitis. Glucocorticosteroids exert anti-inflammatory effects through at least two pathways: the transactivation pathway and the transrepression pathway. Glucocorticosteroids also exert regulatory functions by inducing regulatory cytokines and forkhead box P3 (FoxP3+) regulatory T cells. Evidence suggests that intranasal glucocorticosteroids control not only nasal symptoms but also ocular symptoms. In contrast to sedating H1 receptor antagonists, intranasal glucocorticosteroids can improve impaired performance symptoms, such ...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2773162</comments>
            <pubDate>Wed, 05 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2773162</guid>        </item>
        <item>
            <title>Increased levels of T cell granzyme b in bronchiolitis obliterans syndrome are not suppressed adequately by current immunosuppressive regimens</title>
            <link>http://www.medworm.com/index.php?rid=2773164&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04008.x</link>
            <description>Bronchiolitis obliterans syndrome (BOS) is characterized by persistent alloreactive, infective and non-specific epithelial injury, loss of epithelial integrity and dysregulated repair. We have reported increased apoptosis of epithelial cells collected from the large airway in lung transplant recipients. As part of the alloreactive response, T cells induce apoptosis of target epithelial cells by secreting granzyme b. We hypothesized that granzyme b would be increased in lung transplant patients with acute rejection and BOS and that commonly used immunosuppressive agents would fail to suppress this serine protease adequately. We investigated intracellular T cell granzyme b in blood, bronchoalveolar lavage (BAL) and large airway brushing (23 controls, 29 stable transplant, 23 BOS, 28 acute re...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2773164</comments>
            <pubDate>Sun, 02 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2773164</guid>        </item>
        <item>
            <title>Human papillomavirus 16-specific T cell responses in classic HPV-related vulvar intra-epithelial neoplasia. Determination of strongly immunogenic regions from E6 and E7 proteins</title>
            <link>http://www.medworm.com/index.php?rid=2905760&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04006.x</link>
            <description>Cell-mediated immunity directed against human papillomavirus 16 (HPV-16) antigens was studied in 16 patients affected with classic vulvar intra-epithelial neoplasia (VIN), also known as bowenoid papulosis (BP). Ten patients had blood lymphocyte proliferative T cell responses directed against E6/2 (14[ndash]34) and/or E6/4 (45[ndash]68) peptides, which were identified in the present study as immunodominant among HPV-16 E6 and E7 large peptides. Ex vivo enzyme-linked immunospot[ndash]interferon (IFN)-[gamma] assay was positive in three patients who had proliferative responses. Twelve months later, proliferative T cell responses remained detectable in only six women and the immunodominant antigens remained the E6/2 (14[ndash]34) and E6/4 (45[ndash]68) peptides. The latter large fragments of p...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2905760</comments>
            <pubDate>Wed, 29 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2905760</guid>        </item>
        <item>
            <title>BAFF: a local and systemic target in autoimmune diseases</title>
            <link>http://www.medworm.com/index.php?rid=2773165&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04007.x</link>
            <description>BAFF (B lymphocyte activating factor of the tumour necrosis factor family) is a vital homeostatic cytokine for B cells that helps regulate both innate and adaptive immune responses. Increased serum levels of BAFF are found in a number of different autoimmune diseases, and BAFF is found in inflammatory sites in which there is lymphoid neogenesis. BAFF antagonism has been used in several autoimmune disease models, resulting in B cell depletion, decreased activation of T cells and dendritic cells (DC) and a reduction in the overall inflammatory burden. BAFF, through its interaction with BAFF-R, is required for survival of late transitional, marginal zone and mature naive B cells, all of which are depleted by BAFF blockade. Through their interactions with TACI (transmembrane activator and calc...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2773165</comments>
            <pubDate>Wed, 29 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2773165</guid>        </item>
        <item>
            <title>Activating and inhibitory killer immunoglobulin-like receptors (KIR) in haploidentical haemopoietic stem cell transplantation to cure high-risk leukaemias</title>
            <link>http://www.medworm.com/index.php?rid=2641968&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03983.x</link>
            <description>A number of experimental studies have shown that natural killer (NK) cells can eliminate cancer cells and the mechanisms involved in this effect have been uncovered during the last two decades. Clinical data from haploidentical haematopoietic stem cell transplantation (haplo-HSCT) revealed that NK cells were responsible for remarkably favourable effects in both adult and paediatric high-risk leukaemias. NK receptors specific for major histocompatibility complex (MHC) class I molecules, including killer immunoglobulin (Ig)-like receptors (KIR) and CD94/NKG2A, play a major role in the anti-leukaemia effect (mediating either inhibitory or activating signals). Haplo- HSCT requires a heavy conditioning regimen for the patient and the use of large numbers of T cell-depleted HSC to be grafted. Af...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2641968</comments>
            <pubDate>Tue, 28 Jul 2009 10:34:41 +0100</pubDate>
            <guid isPermaLink="false">2641968</guid>        </item>
        <item>
            <title>Corrigendum</title>
            <link>http://www.medworm.com/index.php?rid=2641985&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04002_3.x</link>
            <description>(Source: Clinical and Experimental Immunology)</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2641985</comments>
            <pubDate>Sun, 26 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2641985</guid>        </item>
        <item>
            <title>Corrigendum</title>
            <link>http://www.medworm.com/index.php?rid=2641984&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04002_2.x</link>
            <description>(Source: Clinical and Experimental Immunology)</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2641984</comments>
            <pubDate>Sun, 26 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2641984</guid>        </item>
        <item>
            <title>Corrigendum</title>
            <link>http://www.medworm.com/index.php?rid=2641983&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04002_1.x</link>
            <description>(Source: Clinical and Experimental Immunology)</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2641983</comments>
            <pubDate>Sun, 26 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2641983</guid>        </item>
        <item>
            <title>Chronic antigenic stimuli as a possible explanation for the immunodepression caused by liver cirrhosis</title>
            <link>http://www.medworm.com/index.php?rid=2773166&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04005.x</link>
            <description>In conclusion, patients with liver cirrhosis showed an intensive activation state with a higher percentage of cells committed to activation-induced death, even in non-advanced stages. It is possible that bacterial permeability and endotoxaemia contribute to the expansion of those lymphocyte populations implicated in the prevention of a more severe antigen-induced immunopathology. (Source: Clinical and Experimental Immunology)</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2773166</comments>
            <pubDate>Wed, 22 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2773166</guid>        </item>
        <item>
            <title>Increased immunoglobulin A in alcoholic liver cirrhosis: exploring the response of B cells to Toll-like receptor 9 activation</title>
            <link>http://www.medworm.com/index.php?rid=2759316&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04004.x</link>
            <description>Alcoholic liver cirrhosis (ALC) is characterized by increased circulating levels of immunoglobulins (Igs). ALC patients undergo bacterial translocation evidenced by the presence of bacterial DNA in peripheral blood. Bacterial pathogen-associated molecular patterns (PAMPs), such as lipopolysaccharide (LPS), peptidoglycan (PGN) and unmethylated cytosine-guanine dinucleotide (CpG) DNA are ligands of Toll-like receptor (TLR)-4, TLR-2 and TLR-9, respectively. Although TLR activation results generally in the secretion of proinflammatory cytokines, activation of B cells through TLR-7 or TLR-9 is involved in their maturation and Ig synthesis. The aim of the present study was to assess Ig synthesis by ALC B cells under PAMP activation in order to evaluate the possible involvement of TLR pathways in...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2759316</comments>
            <pubDate>Sun, 19 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2759316</guid>        </item>
        <item>
            <title>The Tat-conjugated N-terminal region of mucin antigen 1 (MUC1) induces protective immunity against MUC1-expressing tumours</title>
            <link>http://www.medworm.com/index.php?rid=2773168&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03997.x</link>
            <description>Mucin antigen 1 (MUC1) is overexpressed on various human adenocarcinomas and haematological malignancies and has long been used as a target antigen for cancer immunotherapy. Most of the preclinical and clinical studies using MUC1 have used the tandem repeat region of MUC1, which could be presented by only a limited set of major histocompatibility complex haplotypes. Here, we evaluated N-terminal region (2[ndash]147 amino acids) of MUC1 (MUC1-N) for dendritic cell (DC)-based cancer immunotherapy. We used Esherichia coli-derived MUC1-N that was fused to the protein transduction domain of human immunodeficiency virus Tat protein for three reasons. First, mature DCs do not phagocytose soluble protein antigens. Secondly, tumour cells express underglycosylated MUC1, which can generate epitopes r...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2773168</comments>
            <pubDate>Thu, 16 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2773168</guid>        </item>
        <item>
            <title>Prolonging microtubule dysruption enhances the immunogenicity of chronic lymphocytic leukaemia cells</title>
            <link>http://www.medworm.com/index.php?rid=2773167&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04003.x</link>
            <description>Cytotoxic chemotherapies do not usually mediate the expression of an immunogenic gene programme in tumours, despite activating many of the signalling pathways employed by highly immunogenic cells. Concomitant use of agents that modulate and complement stress-signalling pathways activated by chemotherapeutic agents may then enhance the immunogenicity of cancer cells, increase their susceptibility to T cell-mediated controls and lead to higher clinical remission rates. Consistent with this hypothesis, the microtubule inhibitor, vincristine, caused chronic lymphocytic leukaemia (CLL) cells to die rapidly, without increasing their immunogenicity. Protein kinase C (PKC) agonists (such as bryostatin) delayed the death of vincristine-treated CLL cells and made them highly immunogenic, with increa...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2773167</comments>
            <pubDate>Thu, 16 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2773167</guid>        </item>
        <item>
            <title>Intravenous immunoglobulin preparations have no direct effect on B cell proliferation and immunoglobulin production</title>
            <link>http://www.medworm.com/index.php?rid=2759314&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03996.x</link>
            <description>Intravenous immunoglobulin (IVIg) is used for treatment of a variety of immunological disorders and in transplantation. As one of its applications in transplantation is the reduction of donor specific antibodies in the circulation, we examined the direct effect of IVIg on essential parameters of human B cell responses in vitro. Purified human B cells, human B cell hybridomas and T cells were cultured in the presence of graded concentrations of IVIg to test its effect on their proliferative capacity. To address the effect of IVIg on immunoglobulin production, we designed a novel technique making use of quantitative polymerase chain reaction to assess IgM and IgG levels. IVIg failed to inhibit proliferation of human B cells and human B cell hybridomas. In contrast, when IVIg was added to T c...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2759314</comments>
            <pubDate>Thu, 16 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2759314</guid>        </item>
        <item>
            <title>Blocking T cell co-stimulation using a CD80 blocking small molecule reduces delayed type hypersensitivity responses in rhesus monkeys</title>
            <link>http://www.medworm.com/index.php?rid=2759313&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03994.x</link>
            <description>Blockade of co-stimulation signals between T cells and antigen-presenting cells could be an important approach for treatment of autoimmune diseases and transplant rejection. Recently a series of small compound inhibitors which bind human CD80 (B7-1) and inhibit T cell co-stimulation has been described. To investigate their potency for clinical use, one of these compounds, RhuDex[trade], was evaluated for reactivity with rhesus monkey CD80. The in vitro biological effect on rhesus monkey lymphocytes, the potency for suppression of an inflammatory recall response and the protein-induced delayed type hypersensitivity (DTH) response in the skin were studied. In a rhesus monkey T cell co-stimulation assay RhuDex[trade] inhibited proinflammatory cytokine release and cellular proliferation with m...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2759313</comments>
            <pubDate>Thu, 16 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2759313</guid>        </item>
        <item>
            <title>Reciprocal effect of mesenchymal stem cell on experimental autoimmune encephalomyelitis is mediated by transforming growth factor-&amp;#x03B2; and interleukin-6</title>
            <link>http://www.medworm.com/index.php?rid=2759307&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03995.x</link>
            <description>In this report we demonstrate that MSCs have the capacity for either stimulating or inhibiting myelin basic protein-specific T lymphocytes in a dose-dependent manner and modulate antigen-stimulated T cells to differentiate into either T helper type 17 or regulatory T cells, respectively, via pathways involving transforming growth factor-[beta] and interleukin-6. These results may lead better utility of MSCs as a treatment for autoimmune disease. (Source: Clinical and Experimental Immunology)</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2759307</comments>
            <pubDate>Thu, 16 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2759307</guid>        </item>
        <item>
            <title>T-bet and pSTAT-1 expression in PBMC from coeliac disease patients: new markers of disease activity</title>
            <link>http://www.medworm.com/index.php?rid=2759315&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03999.x</link>
            <description>Coeliac disease (CD) is considered a T cell-mediated autoimmune disease, and up-regulation of T-bet and phosphorylated signal transducers and activators of transcription (pSTAT)1, key transcription factors for the development of T helper type 1 (Th1) cells, has been described in the mucosa of patients with untreated CD. Using transcription factor analysis, we investigated whether T-bet and pSTAT1 expressions are up-regulated in the peripheral blood of CD patients and correlate with disease activity. Using flow cytometry, we analysed T-bet, pSTAT1 and pSTAT3 expression in CD4+, CD8+ T cells, CD19+ B cells and monocytes from peripheral blood of 15 untreated and 15 treated CD patients and 30 controls, and longitudinally in five coeliac patients before and after dietary treatment. We evaluated...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2759315</comments>
            <pubDate>Tue, 14 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2759315</guid>        </item>
        <item>
            <title>Mycobacterial antigen-induced T helper type 1 (Th1) and Th2 reactivity of peripheral blood mononuclear cells from diabetic and non-diabetic tuberculosis patients and Mycobacterium bovis bacilli Calmette&amp;#x2013;Gu&amp;eacute;rin (BCG)-vaccinated healthy subjects</title>
            <link>http://www.medworm.com/index.php?rid=2759310&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04000.x</link>
            <description>Patients with diabetes mellitus are more susceptible to tuberculosis (TB), and the clinical conditions of diabetic TB patients deteriorate faster than non-diabetic TB patients, but the immunological basis for this phenomenon is not understood clearly. Given the role of cell-mediated immunity (CMI) in providing protection against TB, we investigated whether CMI responses in diabetic TB patients are compromised. Peripheral blood mononuclear cells (PBMC) obtained from diabetic TB patients, non-diabetic TB patients and Mycobacterium bovis bacilli Calmette[ndash]Guérin (BCG)-vaccinated healthy subjects were cultured in the presence of complex mycobacterial antigens and pools of M. tuberculosis regions of difference (RD)1, RD4, RD6 and RD10 peptides. The PBMC were assessed for antigen-induced c...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2759310</comments>
            <pubDate>Tue, 14 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2759310</guid>        </item>
        <item>
            <title>Vitamin D and respiratory health</title>
            <link>http://www.medworm.com/index.php?rid=2759304&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.04001.x</link>
            <description>Vitamin D is now known to be of physiological importance outside of bone health and calcium homeostasis, and there is mounting evidence that it plays a beneficial role in the prevention and/or treatment of a wide range of diseases. In this brief review the known effects of vitamin D on immune function are described in relation to respiratory health. Vitamin D appears capable of inhibiting pulmonary inflammatory responses while enhancing innate defence mechanisms against respiratory pathogens. Population-based studies showing an association between circulating vitamin D levels and lung function provide strong justification for randomized controlled clinical trials of vitamin D supplementation in patients with respiratory diseases to assess both efficacy and optimal dosage. (Source: Clinical...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2759304</comments>
            <pubDate>Tue, 14 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2759304</guid>        </item>
        <item>
            <title>Cytokine and anti-cytokine therapy in asthma: ready for the clinic?</title>
            <link>http://www.medworm.com/index.php?rid=2759303&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03998.x</link>
            <description>Asthma is a common disease with an increasing prevalence worldwide. Up to 10% of these patients have asthma that is refractory to current therapy. This group have a disproportionate use of health care resources attributed to asthma, have significant morbidity and mortality and therefore represent an unmet clinical need. Asthma is a complex heterogeneous condition that is characterized by typical symptoms and disordered airway physiology set against a background of airway inflammation and remodelling. The inflammatory process underlying asthma is co-ordinated by a cytokine network. Modulating this network with biological therapy presents a new paradigm for asthma treatment. Clinical trials undertaken to date have underscored the complexity of the inflammatory profile and its relationship to...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2759303</comments>
            <pubDate>Tue, 14 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2759303</guid>        </item>
        <item>
            <title>Translational Mini-Review Series on Vaccines for HIV: T lymphocyte trafficking and vaccine-elicited mucosal immunity</title>
            <link>http://www.medworm.com/index.php?rid=2577824&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03927.x</link>
            <description>Many pathogens use mucosal surfaces to enter and propagate within the host, making particularly desirable vaccines that target immune responses specifically to mucosal compartments. The majority of mucosal vaccine design strategies to date have been empirical in nature. However, an emerging body of basic immunological knowledge is providing new insights into the regulation of tissue-specific lymphocyte trafficking and differentiation. These insights afford the opportunity for the rational design of vaccines that focus immune responses at mucosal surfaces. Mucosal cellular immunity may prove critical for protection in the context of HIV infection, and thus there has been considerable interest in developing vaccines that target HIV-specific cellular immune responses to the gastrointestinal a...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2577824</comments>
            <pubDate>Wed, 08 Jul 2009 10:34:31 +0100</pubDate>
            <guid isPermaLink="false">2577824</guid>        </item>
        <item>
            <title>Spatiotemporal expression of chemokines and chemokine receptors in experimental anti-myeloperoxidase antibody-mediated glomerulonephritis</title>
            <link>http://www.medworm.com/index.php?rid=2759319&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03993.x</link>
            <description>In conclusion, expression levels of various chemokines and chemokine receptors were increased in anti-MPO NCGN, and expressed particularly in glomeruli. These chemokines and receptors may serve as potential targets for treatment. Inhibition of a single target, CXCR2, did not attenuate anti-MPO NCGN. Combinatorial interventions may be necessary to avoid redundancy. (Source: Clinical and Experimental Immunology)</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2759319</comments>
            <pubDate>Tue, 07 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2759319</guid>        </item>
        <item>
            <title>Airway-specific recruitment of T cells is reduced in a CD26-deficient F344 rat substrain</title>
            <link>http://www.medworm.com/index.php?rid=2759318&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03991.x</link>
            <description>In conclusion, this is the first report showing a differential site-specific recruitment of T cells to the bronchi in a CD26-deficient rat substrain during an asthma-like inflammation. (Source: Clinical and Experimental Immunology)</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2759318</comments>
            <pubDate>Sun, 28 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2759318</guid>        </item>
        <item>
            <title>Multi-nucleated giant cell formation from human cord blood monocytes in vitro, in comparison with adult peripheral blood monocytes</title>
            <link>http://www.medworm.com/index.php?rid=2759312&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03990.x</link>
            <description>Multi-nucleated giant cells (MGCs; Langhans-type cell), formed from macrophage fusion, are recognized as a hallmark histological feature in chronic inflammation. However, their precise pathological role is still poorly understood, especially for microorganism pathogens in the neonatal immune system, which are capable of surviving intracellularly in phagocytes. To conduct a partial evaluation of the monocyte function of neonates, we investigated the ability of human cord blood monocytes to form MGCs in vitro by stimulating various cytokines and comparing them with adult peripheral blood monocytes. Monocytes from cord blood and adult peripheral blood were isolated and cultured for 14 days with cytokines known to induce MGC in vitro. The fusion index in experiments with a combination of inter...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2759312</comments>
            <pubDate>Mon, 22 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2759312</guid>        </item>
        <item>
            <title>Conserved T cell and natural killer cell function in treatment-experienced adults receiving tenofovir plus didanosine as nucleoside reverse transcription inhibitor backbone</title>
            <link>http://www.medworm.com/index.php?rid=2759309&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03988.x</link>
            <description>Anti-retroviral treatment (ART) usually results in efficient control of virus replication and in immune reconstitution. Among potential adverse effects, impairment of immune responses in terms of CD4+ T cell counts has been attributed to some ART regimens, as with didanosine[ndash]tenofovir. We studied the functional integrity of adaptive and innate immunity during didanosine[ndash]tenofovir-containing ART. Two groups of extensively pretreated patients completing at least 48 weeks of ART containing either lamivudine[ndash]didanosine (n = 21) or tenofovir[ndash]didanosine (n = 25) were identified. In addition to standard clinical immune and virological parameters, we performed a flow cytometric analysis of natural killer (NK) cells, of memory and naive CD4+ T cells and of T cell receptor [a...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2759309</comments>
            <pubDate>Mon, 22 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2759309</guid>        </item>
        <item>
            <title>Coagulation activation in autoimmune bullous diseases</title>
            <link>http://www.medworm.com/index.php?rid=2759306&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03989.x</link>
            <description>The main autoimmune blistering skin disorders are pemphigus vulgaris (PV) and bullous pemphigoid (BP). They differ in the inflammatory infiltrate, which is more intense in BP. Inflammation is known to activate coagulation in several disorders. Local and systemic activation of coagulation was evaluated in BP and PV. We studied 20 BP patients (10 active and 10 remittent), 23 PV patients (13 active and 10 remittent) and 10 healthy subjects. The coagulation markers prothrombin fragment F1+2 and D-dimer were measured by enzyme-immunoassays in plasma. The presence of tissue factor (TF), the main initiator of blood coagulation, was evaluated immunohistochemically in skin specimens from 10 patients with active PV, 10 patients with active BP and 10 controls. Plasma F1+2 and D-dimer levels were sign...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2759306</comments>
            <pubDate>Mon, 22 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2759306</guid>        </item>
        <item>
            <title>Glucocorticoid treatment restores the impaired suppressive function of regulatory T cells in patients with relapsing&amp;#x2013;remitting multiple sclerosis</title>
            <link>http://www.medworm.com/index.php?rid=2759305&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03987.x</link>
            <description>In conclusion, GC treatment restores the impaired Treg function in patients with RR-MS in its acute phase. (Source: Clinical and Experimental Immunology)</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2759305</comments>
            <pubDate>Mon, 22 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2759305</guid>        </item>
        <item>
            <title>Glucocorticoid sensitivity of lipopolysaccharide-stimulated chronic obstructive pulmonary disease alveolar macrophages</title>
            <link>http://www.medworm.com/index.php?rid=2759311&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03986.x</link>
            <description>The objective of this study was to identify Gc-insensitive inflammatory mediators produced by lipopolysaccharide (LPS)-stimulated alveolar macrophages from COPD patients. LPS-stimulated alveolar macrophages from 15 COPD patients, nine smokers (S) and nine healthy non-smokers (HNS) were stimulated with LPS with or without dexamethasone (100 and 1000 nM). Luminex and enzyme-linked immunosorbent assay were used to measure 23 inflammatory mediators. After LPS stimulation there were lower levels of inflammatory mediators in COPD patients and S compared to HNS. There was no difference between groups for the effects of dexamethasone at either concentration (P &gt; 0·05 for all comparisons). Tumour necrosis factor (TNF)-[alpha], interleukin (IL)-6 and growth-related oncogene (GRO)-[alpha] displayed ...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2759311</comments>
            <pubDate>Tue, 16 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2759311</guid>        </item>
        <item>
            <title>Impaired activation of Stat1 and c-Jun as a possible defect in macrophages of patients with active tuberculosis</title>
            <link>http://www.medworm.com/index.php?rid=2759308&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03985.x</link>
            <description>Studies of patients with active tuberculosis (TB) and infected healthy individuals have shown that interferon (IFN)-[gamma] is present in sites of Mycobacterium tuberculosis infection in comparable levels. This suggests that there is a deficiency in the macrophage response to IFN-[gamma] in TB patients. We used recombinant human IFN-[gamma] to stimulate adherent monocyte-derived macrophages from three groups of people: patients with active tuberculosis (TBP), their healthy household contacts (HHC) and healthy uninfected controls from the community (CC). We then evaluated the ability of the macrophages to inhibit the growth of M. tuberculosis H37Rv as well as their cytokine profile at early in infection (48 h). After IFN-[gamma] treatment, macrophages of healthy individuals (HHC and CC) con...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2759308</comments>
            <pubDate>Wed, 10 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2759308</guid>        </item>
        <item>
            <title>Clinical experience with Flebogamma&amp;reg; 5% DIF: a new generation of intravenous immunoglobulins in patients with primary immunodeficiency disease</title>
            <link>http://www.medworm.com/index.php?rid=2470052&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03951.x</link>
            <description>The development of effective, safe, liquid intravenous immunoglobulins (IVIG) preparations has represented a major therapeutic advancement in the treatment of patients with antibody deficiencies. Flebogamma® 5% was the first liquid IVIG licensed in Europe that has been widely used in the treatment of immunodeficiency diseases. It has been proven to have an excellent efficacy and safety profile. Flebogamma® 5% dual inactivation and filtration (DIF) is a newly developed IVIG preparation that shares formulation characteristics and identical biochemical and stability profiles with Flebogamma® 5%. In addition to pasteurization, already performed in Flebogamma® 5%, solvent-detergent treatment and sequential nanofiltration through filters with pore sizes of 35 nm followed by 20 nm have been a...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2470052</comments>
            <pubDate>Wed, 10 Jun 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2470052</guid>        </item>
        <item>
            <title>Flebogamma&amp;reg; 5% DIF development: rationale for a new option in intravenous immunoglobulin therapy</title>
            <link>http://www.medworm.com/index.php?rid=2470051&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03953.x</link>
            <description>Flebogamma® 5% dual inactivation and filtration (DIF), a new 5% liquid intravenous immunoglobulin with a stability of 2 years when stored at temperatures between 2 and 30°C, has been developed. This new product is the result of the accumulated experience provided by Flebogamma®, with more than 30 million grams administered since 1992 in Europe and the United States, and the implementation of the latest technology to improve Flebogamma® even more by increasing its viral safety margin further. In addition to the specific inactivation stage for Flebogamma® 5% (pasteurization), the new process includes a solvent[ndash]detergent treatment and nanofiltration through a Planova filter down to 20 nm. The preparation presents a mean purity of 99·6 ± 0·2% with a correct chromatographic profil...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2470051</comments>
            <pubDate>Wed, 10 Jun 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2470051</guid>        </item>
        <item>
            <title>Lung disease, antibodies and other unresolved issues in immune globulin therapy for antibody deficiency</title>
            <link>http://www.medworm.com/index.php?rid=2470050&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03952.x</link>
            <description>Defects of antibody production are the most common of the primary immune defects of man. While these defects have been described in clinical terms for more than five decades, in most cases, the pathogenesis is still poorly understood. The most common clinically important of these is common variable immune deficiency. However there is no strict definition of this defect and the criteria for initiating immune globulin therapy are not standardized, leading to wide variation in treatment practices. In addition there has been no clear means to adequate assess progression of lung disease or elucidate the causes of progressive pulmonary inflammation found in some subjects. Moreover, there are still questions such as what are the best predictors of chronic lung disease and how can we prevent this ...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2470050</comments>
            <pubDate>Wed, 10 Jun 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2470050</guid>        </item>
        <item>
            <title>The European internet-based patient and research database for primary immunodeficiencies: results 2006&amp;#x2013;2008</title>
            <link>http://www.medworm.com/index.php?rid=2470049&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03954.x</link>
            <description>Primary immunodeficiencies (PID) are rare diseases; therefore transnational studies are essential to maximize the scientific outcome and to improve diagnosis and therapy. In order to estimate the prevalence of PID in Europe as well as to establish and evaluate harmonized guidelines for the diagnosis and treatment of PID, the European Society for Immunodeficiencies (ESID) has developed an internet-based database for clinical and research data on patients with PID. This database is a platform for epidemiological analyses as well as the development of new diagnostic and therapeutic strategies and the identification of novel disease-associated genes. Within 4 years, 7430 patients from 39 countries have been documented in the ESID database. Common variable immunodeficiency (CVID) represents the...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2470049</comments>
            <pubDate>Wed, 10 Jun 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2470049</guid>        </item>
        <item>
            <title>Mannose-binding lectin is present in human semen and modulates cellular adhesion of Neisseria gonorrhoeae in vitro</title>
            <link>http://www.medworm.com/index.php?rid=2641979&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03984.x</link>
            <description>In this study MBL was found to be present at a low concentration in semen samples in the range 1·2[ndash]24·9 ng/ml. Co-incubation of bacteria with semen resulted in the binding of MBL to the bacterial surface. Neisseria gonorrhoeae is a common cause of genitourinary infection. MBL bound to N. gonorrhoeae with strain-to-strain variation in the intensity of binding and nature of the bacterial receptor. Pretreatment with MBL concentrations similar to those found in human serum modulated the adhesion of N. gonorrhoeae strain FA1090 but not strain MS11 to epithelial cells. This effect was dose-dependent. This work demonstrates that MBL is present in human semen and modifies cellular responses to N. gonorrhoeae in a concentration-dependent manner. (Source: Clinical and Experimental Immunology...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2641979</comments>
            <pubDate>Mon, 08 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2641979</guid>        </item>
        <item>
            <title>Mechanisms of action of immune globulin</title>
            <link>http://www.medworm.com/index.php?rid=2470048&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03955.x</link>
            <description>(Source: Clinical and Experimental Immunology)</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2470048</comments>
            <pubDate>Mon, 01 Jun 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2470048</guid>        </item>
        <item>
            <title>CCR5 blockade in combination with rapamycin prolongs cardiac allograft survival in mice</title>
            <link>http://www.medworm.com/index.php?rid=2641982&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03982.x</link>
            <description>In this study we examined the inhibition of CCR5 in combination with the treatment with rapa in cardiac transplantation. Fully major histocompatibility complex-mismatched murine cardiac allograft models were randomized to five groups. They were administered with anti-CCR5 antibody or control antibody and rapa or phosphate-buffered saline (PBS), respectively. An additional group was treated with anti-CCR5 antibody, rapa and anti-CD25 antibody. Allograft rejection was investigated by flow cytometric analyses and enzyme-linked immunospot assay. Allografts treated with anti-CCR5 antibody plus rapa showed significantly prolonged survival (83 ± 3 days, P &lt; 0·001) compared with control antibody plus PBS-treated allografts (6 ± 1 days). Treatment with anti-CCR5 monoclonal antibody (mAb) plus ra...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2641982</comments>
            <pubDate>Mon, 25 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2641982</guid>        </item>
        <item>
            <title>Homeostatic chemokines CCL19 and CCL21 promote inflammation in human immunodeficiency virus-infected patients with ongoing viral replication</title>
            <link>http://www.medworm.com/index.php?rid=2641978&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03976.x</link>
            <description>We examined the expression of CCL19 and CCL21 in mononuclear cells from peripheral blood mononuclear cells (PBMC) and bone marrow mononuclear cells (BMMC) in HIV-infected patients before and during highly active anti-retroviral therapy (HAART). We also examined the ability of CCL19/CCL21 to promote inflammatory responses in these patients. PBMC from untreated HIV-infected patients (n = 29) released enhanced levels of CCL19 spontaneously compared with cells from controls (n = 20), particularly in those with symptomatic disease (n = 15, P &lt; 0·01 versus controls). During HAART (n = 9), there was a decrease in the spontaneous CCL19 release and an increase in the phytohaemagglutinin-stimulated CCL19 release in both PBMC (P &lt; 0·01) and BMMC (P &lt; 0·05). In patients with enhanced HIV replicatio...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2641978</comments>
            <pubDate>Tue, 19 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2641978</guid>        </item>
        <item>
            <title>Functional and clinical consequences of Fc receptor polymorphic and copy number variants</title>
            <link>http://www.medworm.com/index.php?rid=2577833&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03980.x</link>
            <description>Receptors for immunoglobulins (Fc receptors) play a central role during an immune response, as they mediate the specific recognition of antigens of almost infinite diversity by leucocytes, thereby linking the humoral and cellular components of immunity. Indeed, engagement of Fc receptors by immunoglobulins initiates a range of immunoregulatory processes that might also play a role in disease pathogenesis. In the circulation, five main types of immunoglobulins (Ig) exist [ndash] namely IgG, IgA, IgE, IgM and IgD and receptors with the ability to recognize and bind to IgG (Fc[gamma] receptor family), IgE (Fc[epsilon]RI and CD23), IgA (CD89; Fc[alpha]/µR) and IgM (Fc[alpha]/µR) have been identified and characterized. However, it is astonishing that nearly all the known human Fc receptors di...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2577833</comments>
            <pubDate>Tue, 19 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2577833</guid>        </item>
        <item>
            <title>Translational Mini-Review Series on B Cell-Directed Therapies: Recent advances in B cell-directed biological therapies for autoimmune disorders</title>
            <link>http://www.medworm.com/index.php?rid=2577828&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03979.x</link>
            <description>B cell-directed therapies are promising treatments for autoimmune disorders. Besides targeting CD20, newer B cell-directed therapies are in development that target other B cell surface molecules and differentiation factors. An increasing number of B cell-directed therapies are in development for the treatment of autoimmune disorders. Like rituximab, which is approved as a treatment for rheumatoid arthritis (RA), many of these newer agents deplete B cells or target pathways essential for B cell development and function; however, many questions remain about their optimal use in the clinic and about the role of B cells in disease pathogenesis. Other therapies besides rituximab that target CD20 are the furthest along in development. Besides targeting CD20, the newer B cell-directed therapies t...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2577828</comments>
            <pubDate>Tue, 19 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2577828</guid>        </item>
        <item>
            <title>Translational Mini-Review Series on B Cell-Directed Therapies: The pathogenic role of B cells in autoantibody-associated autoimmune diseases &amp;#x2013; lessons from B cell-depletion therapy</title>
            <link>http://www.medworm.com/index.php?rid=2577827&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03978.x</link>
            <description>B cell depletion therapy with rituximab (BCDT) is a licensed treatment for rheumatoid arthritis and has shown promising results in the treatment of severe, refractory patients with other autoantibody-associated autoimmune diseases (AAID). The exact role that B cells play in the pathogenesis of AAID and consequently the mechanisms by which BCDT is effective are not known. The two more widely discussed hypotheses are that BCDT is effective because it removes the precursors of plasma cells producing pathogenic autoantibody species, or because it depletes a critical mass of autoreactive B cell clones that present antigen to pathogenic autoreactive T cells. This review will focus on the effects of BCDT and whether the response of patients with AAID to BCDT could be due ultimately to its effects...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2577827</comments>
            <pubDate>Tue, 19 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2577827</guid>        </item>
        <item>
            <title>Translational Mini-Review Series on B Cell-Directed Therapies: B cell-directed therapy for autoimmune diseases</title>
            <link>http://www.medworm.com/index.php?rid=2577826&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03977.x</link>
            <description>B cells play an important role in the pathogenesis of both systemic and organ-specific autoimmune diseases. Autoreactive B cells not only produce autoantibodies, but are also specialized to present specific autoantigens efficiently to T cells. Furthermore, these B cells can secrete proinflammatory cytokines and can amplify the vicious cycle of self-destruction. Thus, B cell-directed therapies are potentially an important approach for treating autoimmune diseases. On the other hand, like T cells, there are subsets of B cells that produce anti-inflammatory cytokines and are immunosuppressive. These regulatory B cell subsets can protect against and ameliorate autoimmune diseases. Thus targeting B cells therapeutically will require this balance to be considered. Here we summarize the roles of ...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2577826</comments>
            <pubDate>Tue, 19 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2577826</guid>        </item>
        <item>
            <title>Exaggerated inflammatory response of primary human myeloid dendritic cells to lipopolysaccharide in patients with inflammatory bowel disease</title>
            <link>http://www.medworm.com/index.php?rid=2641981&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03981.x</link>
            <description>Inflammatory bowel disease (IBD) results from a breakdown of tolerance towards the indigenous flora in genetically susceptible hosts. Failure of dendritic cells (DC) to interpret molecular microbial patterns appropriately when directing innate and adaptive immune responses is conceivable. Primary (conventional, non-monocyte generated) CD1c+CD11c+CD14-CD16-CD19- myeloid blood or mucosal dendritic cells (mDC) from 76 patients with Crohn's disease (CD) or ulcerative colitis (UC) in remission, during flare-ups (FU) and 76 healthy or non-IBD controls were analysed by fluorescence activated cell sorter (FACS) flow cytometry and real-time polymerase chain reaction. Cytokine secretion of freshly isolated, cultured and lipopolysaccharide (LPS)-stimulated highly purified mDC (purity &gt;95%) was assess...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2641981</comments>
            <pubDate>Thu, 14 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2641981</guid>        </item>
        <item>
            <title>Ficolin 2 (FCN2) functional polymorphisms and the risk of rheumatic fever and rheumatic heart disease</title>
            <link>http://www.medworm.com/index.php?rid=2641977&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03975.x</link>
            <description>Ficolins are pattern-recognition proteins involved in innate immunity, which upon binding to their specific pathogen-associated molecular patterns on the microbial surfaces trigger the immune response either by binding to collectin cellular receptors or by initiating the complement lectin pathway. In humans, three ficolin genes have been identified, which encode ficolin-1 (M-ficolin), ficolin-2 (L-ficolin) and ficolin-3 (H-ficolin or Hakata antigen). Ficolin-2 was shown to bind to lipoteichoic acid, a cell wall constituent in all Gram-positive bacteria such as Streptococcus pyogenes, which is the aetiological agent of rheumatic fever (RF) and its most severe sequelae, chronic rheumatic heart disease (CRHD). Here we investigated polymorphisms in the promoter region of the FCN2 gene (at posi...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2641977</comments>
            <pubDate>Thu, 14 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2641977</guid>        </item>
        <item>
            <title>CD3 expression distinguishes two &amp;#x03B3;&amp;#x03B4;T cell receptor subsets with different phenotype and effector function in tuberculous pleurisy</title>
            <link>http://www.medworm.com/index.php?rid=2641976&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03974.x</link>
            <description>Tuberculous pleurisy is a naturally occurring site of Mycobacterium tuberculosis (Mtb) infection. Herein, we describe the expression of activation, natural killer (NK) and cell migration markers, as well as effector functions from [gamma][delta]T cells in peripheral blood (PB) and pleural effusion (PE) from tuberculosis patients (TB). We observed a decreased percentage of circulating [gamma][delta]T from TB patients and differential expression of NK as well as of chemokine receptors on PB and PE. Two subsets of [gamma][delta]T cells were differentiated by the CD3/[gamma][delta]T cell receptor ([gamma][delta]TCR) complex. The [gamma][delta]TCRlow subset had a higher CD3 to TCR ratio and was enriched in V[delta]2+ cells, whereas most V[delta]1+ cells belonged to the [gamma][delta]TCRhigh sub...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2641976</comments>
            <pubDate>Thu, 14 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2641976</guid>        </item>
        <item>
            <title>Expression and regulation of the NALP3 inflammasome complex in periodontal diseases</title>
            <link>http://www.medworm.com/index.php?rid=2641980&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03972.x</link>
            <description>In conclusion, this study reveals a role for the NALP3 inflammasome complex in inflammatory periodontal disease, and provides a mechanistic insight to the host immune responses involved in the pathogenesis of the disease by demonstrating the modulation of this cytokine-signalling pathway by bacterial challenge. (Source: Clinical and Experimental Immunology)</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2641980</comments>
            <pubDate>Tue, 12 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2641980</guid>        </item>
        <item>
            <title>Invariant natural killer (iNK)&amp;nbsp;T cell deficiency in patients with common variable immunodeficiency</title>
            <link>http://www.medworm.com/index.php?rid=2641973&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03973.x</link>
            <description>Common variable immunodeficiency (CVID) is a B cell immunodeficiency disorder characterized frequently by failure of memory B cell development and antibody secretion. A unifying cellular pathogenesis for CVID has not been forthcoming, but given the immunoregulatory role of invariant NK (iNK) T cells and their absence in several other immunodeficiencies, we quantified these cells in the blood of 58 CVID patients. There was a marked decrease in the proportion of iNK T cells in CVID patients compared with controls. This was particularly notable in those with low isotype-switched memory B cells, but subset analysis demonstrated no difference when stratified by specific clinical features. We propose that the decreased proportion of iNK T cells in CVID might be linked to the failure of memory B ...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2641973</comments>
            <pubDate>Tue, 12 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2641973</guid>        </item>
        <item>
            <title>Cancer immunotherapy: co-stimulatory agonists and co-inhibitory antagonists</title>
            <link>http://www.medworm.com/index.php?rid=2399300&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03912.x</link>
            <description>The generation and maintenance of immune responses are controlled by both co-stimulatory and co-inhibitory signalling through T cell co-receptors, many of which belong to the immunoglobulin-like superfamily or the tumour necrosis factor receptor superfamily. Agonistic or antagonistic monoclonal antibodies targeting these co-receptors have the potential to enhance immunity. Furthermore, their activity on the immunosuppressive regulatory T cell populations which are prevalent within many tumours provides an additional rationale for their use as anti-cancer therapies. This review summarizes the interactions between cancer and the immune system, highlighting the ways in which these new classes of immunostimulatory antibodies might enhance anti-tumour immunity and summarizing early clinical exp...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2399300</comments>
            <pubDate>Sun, 10 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2399300</guid>        </item>
        <item>
            <title>The skin homing receptor cutaneous leucocyte-associated antigen (CLA) is up-regulated by Leishmania antigens in T lymphocytes during active cutaneous leishmaniasis</title>
            <link>http://www.medworm.com/index.php?rid=2641975&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03970.x</link>
            <description>The cutaneous leucocyte-associated antigen receptor (CLA) can direct Leishmania-specific T lymphocytes towards inflamed skin lesions. Homing receptors [CLA, lymphocyte-associated antigen 1 (LFA-1) or CD62L] were analysed in lymphocytes from blood and cutaneous leishmaniasis (CL) lesions. CL patients with active lesions (A-CL) presented lower levels of T lymphocytes expressing the CLA+ phenotype (T CD4+ = 10·4% ± 7·5% and T CD8+ = 5·8% ± 3·4%) than did healthy subjects (HS) (T CD4+ = 19·3% ± 13·1% and T CD8+ = 21·6% ± 8·8%), notably in T CD8+ (P &lt; 0·001). In clinically cured patients these percentages returned to levels observed in HS. Leishmanial antigens up-regulated CLA in T cells (CLA+ in T CD4+ = 33·3% ± 14·1%; CLA+ in T CD8+ = 22·4% ± 9·4%) from A-CL but not from HS...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2641975</comments>
            <pubDate>Tue, 05 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2641975</guid>        </item>
        <item>
            <title>Dexamethasone suppresses interleukin-22 associated with bacterial infection in vitro and in vivo</title>
            <link>http://www.medworm.com/index.php?rid=2641974&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03969.x</link>
            <description>Interleukin (IL)-22 production triggered by innate immune mechanisms has been identified as key to efficient intestinal anti-bacterial host defence and preservation of homeostasis. We hypothesized that glucocorticoid therapy may impair IL-22 expression, which should promote intestinal epithelial damage with the potential of subsequent bacterial translocation. High-dose corticosteroid therapy in Crohn's disease has been associated with an increased rate of abscess formation and ultimately with a higher risk of developing postoperative infectious complications, including abdominal sepsis. Thus, we sought to investigate effects of the prototypic glucocorticoid dexamethasone on IL-22 production in the context of bacterial infection. Enhanced IL-22 plasma levels were detectable in rat sepsis. M...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2641974</comments>
            <pubDate>Tue, 05 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2641974</guid>        </item>
        <item>
            <title>&amp;#x03B2;-Glucosylceramide ameliorates liver inflammation in murine autoimmune cholangitis</title>
            <link>http://www.medworm.com/index.php?rid=2641972&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03971.x</link>
            <description>We have demonstrated spontaneous development of autoimmune cholangitis, similar to human primary biliary cirrhosis, in mice expressing a dominant negative form of the transforming growth factor-[beta] receptor (dnTGF-[beta]RII) restricted to T cells. The autoimmune cholangitis appears to be mediated by autoreactive CD8+ T lymphocytes that home to the portal tracts and biliary system. Because the liver pathology is primarily secondary to CD8+ T cells, we have determined herein whether administration of [beta]-glucosylceramide (GC), a naturally occurring plant glycosphingolipid, alters the natural history of disease in this model. We chose GC because previous work has demonstrated its ability to alter CD8+ T cell responses and to down-regulate tissue inflammation. Accordingly, dnTGF-[beta]RI...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2641972</comments>
            <pubDate>Tue, 05 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2641972</guid>        </item>
        <item>
            <title>Vaccination with collagen-pulsed dendritic cells prevents the onset and reduces the disease severity in the mouse model of spontaneous polychondritis</title>
            <link>http://www.medworm.com/index.php?rid=2641971&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03968.x</link>
            <description>We report here that injection of iDCs pulsed with chick type II collagen (CII) delayed the onset significantly and suppressed the severity of spontaneous polychondritis (SP) in the human leucocyte antigen (HLA)-DQ6[alpha][beta]8[alpha][beta] transgenic mouse model. Bone marrow-derived iDCs were pulsed in vitro with CII and transferred into 6-week-old HLA-DQ6[alpha][beta]8[alpha][beta] transgenic mice. Mice receiving CII-pulsed iDCs did not display any clinical signs of disease until 5·5 months of age, indicating the ability of the DC vaccine to delay significantly the onset of SP. Control groups receiving unpulsed iDCs or phosphate-buffered saline (PBS) developed polyarthritis at 3·5 months, as we have reported previously. The severity and incidence of disease was reduced in mice injecte...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2641971</comments>
            <pubDate>Tue, 05 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2641971</guid>        </item>
        <item>
            <title>The protective role of antibody responses during Mycobacterium tuberculosis infection</title>
            <link>http://www.medworm.com/index.php?rid=2577832&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03967.x</link>
            <description>Tuberculosis (TB) caused by Mycobacterium tuberculosis (Mtb) is one of the most important infectious diseases globally. Immune effector mechanisms that lead to protection or development of clinical disease are not fully known. It is generally accepted that cell-mediated immunity (CMI) plays a pivotal role in controlling Mtb infection, whereas antibody responses are believed to have no protective role. This generalization is based mainly on early classical experiments that lacked standard protocols, and the T helper type 1 (Th1)/Th2 paradigm. According to the Th1/Th2 paradigm Th1 cells protect the host from intracellular pathogens, whereas Th2 cells protect form extracellular pathogens. During the last two decades, the Th1/Th2 paradigm has dominated not only our understanding of immunity to...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2577832</comments>
            <pubDate>Tue, 05 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2577832</guid>        </item>
        <item>
            <title>Cells with regulatory function of the innate and adaptive immune system in primary Sj&amp;ouml;gren's syndrome</title>
            <link>http://www.medworm.com/index.php?rid=2641970&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03966.x</link>
            <description>The aim of the present study was to describe subsets of cells with regulatory properties in primary Sjögren's syndrome (pSS), and to correlate these cell populations with clinical symptoms. Among the 32 investigated patients, 23 had extraglandular manifestations (EGMs), while nine had only glandular symptoms. Twenty healthy individuals served as controls. The percentages of natural killer (NK), natural killer T cells (NK T), interleukin (IL)-10 producing T regulatory type 1 (Tr1) cells and CD4+CD25+ regulatory T cells (Treg) cells were determined by flow cytometry and serum cytokine levels of IL-4, IL-6, IL-10, tumour necrosis factor (TNF)-[alpha] and interferon (IFN)-[gamma] were evaluated by enzyme-linked immunosorbent assay (ELISA). Functional tests were carried out to assess the suppr...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2641970</comments>
            <pubDate>Tue, 28 Apr 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2641970</guid>        </item>
        <item>
            <title>Altered innate immune response of plasmacytoid dendritic cells in multiple sclerosis</title>
            <link>http://www.medworm.com/index.php?rid=2641969&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03964.x</link>
            <description>Plasmacytoid dendritic cells (pDCs) are of crucial importance in immune regulation and response to microbial factors. In multiple sclerosis (MS), pDCs from peripheral blood showed an immature phenotype, but its role in susceptibility to MS is not determined. Because infectious diseases are established triggers of exacerbations in MS, in this study we have characterized the expression of Toll-like receptors (TLR) and the maturation and functional properties of peripheral blood pDCs from clinically stable, untreated MS patients in response to signals of innate immunity. After stimulation of TLR-9, interferon (IFN)-[alpha] production by pDCs was significantly lower in MS (n = 12) compared to healthy controls (n = 9). In an allogenic two-step co-culture assay we found an impaired effect of TLR...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2641969</comments>
            <pubDate>Tue, 28 Apr 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2641969</guid>        </item>
        <item>
            <title>T helper type 17-related cytokine expression is increased in the bronchial mucosa of stable chronic obstructive pulmonary disease patients</title>
            <link>http://www.medworm.com/index.php?rid=2577841&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03965.x</link>
            <description>There are increased numbers of activated T lymphocytes in the bronchial mucosa of stable chronic obstructive pulmonary disease (COPD) patients. T helper type 17 (Th17) cells release interleukin (IL)-17 as their effector cytokine under the control of IL-22 and IL-23. Furthermore, Th17 numbers are increased in some chronic inflammatory conditions. To investigate the expression of interleukin (IL)-17A, IL-17F, IL-21, IL-22 and IL-23 and of retinoic orphan receptor RORC2, a marker of Th17 cells, in bronchial biopsies from patients with stable COPD of different severity compared with age-matched control subjects. The expression of IL-17A, IL-17F, IL-21, IL-22, IL-23 and RORC2 was measured in the bronchial mucosa using immunohistochemistry and/or quantitative polymerase chain reaction. The numbe...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2577841</comments>
            <pubDate>Tue, 28 Apr 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2577841</guid>        </item>
        <item>
            <title>Thalidomide has a therapeutic effect on interstitial lung fibrosis: evidence from in vitro and in vivo studies</title>
            <link>http://www.medworm.com/index.php?rid=2577840&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03962.x</link>
            <description>The objective of this study was to investigate the effects of thalidomide (THD) on interstitial lung fibrosis (ILF). In vitro, human fetal lung fibroblast (HFL-F) to myofibroblast (MF) trans-differentiation was induced by transforming growth factor (TGF)-[beta]1. The effects of THD on trans-differentiation process or differentiated MF were evaluated by measuring hydroxyproline (HYP) content by alkaline hydrolysis colorimetry, [alpha]-smooth muscle actin ([alpha]-SMA) protein by Western blot and [alpha]-SMA and pro-collagen III mRNA expressions by semi-quantitative reverse transcription[ndash]polymerase chain reaction; in vivo, a mouse model of ILF was generated by daily subcutaneous injection of bleomycin (BLM) in female C3H mice. Gastric perfusion of THD began 1 week prior to injection an...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
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            <pubDate>Tue, 21 Apr 2009 23:00:00 +0100</pubDate>
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            <title>Programmed death (PD)-1 molecule and its ligand PD-L1 distribution among memory CD4 and CD8 T cell subsets in human immunodeficiency virus-1-infected individuals</title>
            <link>http://www.medworm.com/index.php?rid=2485478&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03960.x</link>
            <description>This study examines correlations between T cell maturation, expression of PD-1 and PD-L1, and the effects of their blockade. Peripheral blood mononuclear cells (PBMC) from 24 HIV-1+ and 17 uninfected individuals were phenotyped for PD-1 and PD-L1 expression on CD4+ and CD8+ T cell subsets. The effect of PD-1 and PD-L1 blockade on proliferation and interferon (IFN)-[gamma] production was tested on eight HIV-1+ patients. Naive (CCR7+CD45RA+) CD8+ T cells were reduced in HIV-1 aviraemic (P = 0·0065) and viraemic patients (P = 0·0130); CD8 T effector memory subsets [CCR7-CD45RA[ndash](TEM)] were increased in HIV-1+ aviraemic (P = 0·0122) and viraemic (P = 0·0023) individuals versus controls. PD-1 expression was increased in CD4 naive (P = 0·0496), central memory [CCR7+CD45RA[ndash] (TCM);...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2485478</comments>
            <pubDate>Tue, 21 Apr 2009 23:00:00 +0100</pubDate>
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            <title>Attenuation of massive cytokine response to the staphylococcal enterotoxin B superantigen by the innate immunomodulatory protein lactoferrin</title>
            <link>http://www.medworm.com/index.php?rid=2485475&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03963.x</link>
            <description>Staphylococcal enterotoxin B (SEB) is a pyrogenic exotoxin and a potent superantigen which causes massive T cell activation and cytokine secretion, leading to profound immunosuppression and morbidity. The inhibition of SEB-induced responses is thus considered a goal in the management of certain types of staphylococcal infections. Lactoferrin (LF) is a multi-functional glycoprotein with both bacteriostatic and bactericidal activities. In addition, LF is known to have potent immunomodulatory properties. Given the anti-microbial and anti-inflammatory properties of this protein, we hypothesized that LF can modulate T cell responses to SEB. Here, we report that bovine LF (bLF) was indeed able to attenuate SEB-induced proliferation, interleukin-2 production and CD25 expression by human leucocyte...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2485475</comments>
            <pubDate>Tue, 21 Apr 2009 23:00:00 +0100</pubDate>
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            <title>Phenotypic and functional markers for 1&amp;#x03B1;,25-dihydroxyvitamin D3-modified regulatory dendritic cells</title>
            <link>http://www.medworm.com/index.php?rid=2485474&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03961.x</link>
            <description>The clinical use of dendritic cells (DCs) to induce antigen-specific immune tolerance has been hampered by the lack of a widely acknowledged method for generating human regulatory DCs but even more so by the non-existence of reliable markers. Thus, we set out to find reliable markers that can be measured with simple methods to identify regulatory DCs that are applicable for future clinical studies. Human DCs were generated from peripheral blood monocytes in the presence of 1[alpha],25-dihydroxyvitamin D3 (VD3), which gave rise to a phenotype that resembles immature DCs, with the exception of high CD14 and reduced CD1a on the cell surface. These VD3-treated DCs exert a long-lasting inefficient T cell stimulation and induce T cell hyporesponsiveness with regulatory potential. Importantly, su...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2485474</comments>
            <pubDate>Tue, 21 Apr 2009 23:00:00 +0100</pubDate>
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            <title>Immunomodulation of innate immune responses by vasoactive intestinal peptide (VIP): its therapeutic potential in inflammatory disease</title>
            <link>http://www.medworm.com/index.php?rid=2577831&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03956.x</link>
            <description>Since the late 1970s a number of laboratories have studied the role of vasoactive intestinal peptide (VIP) in inflammation and immunity. These studies have highlighted the dramatic effect of VIP on immune cell activation and function, and studies using animal models of disease have indicated that VIP has significant therapeutic and prophylactic potential. This review will focus on the effects of VIP on innate immune cell function and discuss the therapeutic potential for VIP in inflammatory diseases of humans. (Source: Clinical and Experimental Immunology)</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2577831</comments>
            <pubDate>Tue, 14 Apr 2009 23:00:00 +0100</pubDate>
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            <title>Enhanced complement activation is part of the unfavourable cardiovascular risk profile in South Asians</title>
            <link>http://www.medworm.com/index.php?rid=2485479&amp;cid=s_33580_3_f&amp;fid=33580&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1365-2249.2009.03959.x</link>
            <description>South Asian immigrants in western societies exhibit a high burden of diabetes and subsequent vascular complications. Diabetic vascular complications are associated with vascular inflammation. We hypothesize that enhanced complement activation is involved. Therefore, levels of complement C3 and SC5b-9 [ndash] the soluble end product of complement activation [ndash] in a group of 200 South Asians were compared with an age- and sex-matched control group of native Caucasians. In addition, the association between complement levels and albuminuria, an indicator of renal damage and a cardiovascular risk marker, was assessed in the diabetic South Asian group. Compared with native Caucasians, South Asians had significantly higher levels of both serum C3 and plasma SC5b-9, even when only non-diabeti...</description>
            <author>Clinical and Experimental Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2485479</comments>
            <pubDate>Tue, 14 Apr 2009 23:00:00 +0100</pubDate>
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