30 research outputs found

    A double-blind trial of transfer factor vs placebo in multiple sclerosis patients.

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    A double-blind trial of the effect of transfer factor on multiple sclerosis patients was carried out. In a series of fifty-six multiple sclerosis patients treated with monthly injections of either transfer factor or placebo for 1 year, no beneficial effect of transfer factor was noted. In addition, none of the immunological and serological parameters studied (measles migration inhibition, measles HI titre or CSF immunoglobulin) changed as a result of transfer factor therapy. Histocompatibility typing and CSF IgG/TP ratios were correlated with the disease activity. Of interest was the finding that the presence of the DW2 antigen, when unassociated with HLA-B7 antigen, appeared to correlate with the mildest form of disease activity

    Species-Specific Traits Rather Than Resource Partitioning Mediate Diversity Effects on Resource Use

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    Background: The link between biodiversity and ecosystem processes has firmly been established, but the mechanisms underpinning this relationship are poorly documented. Most studies have focused on terrestrial plant systems where resource use can be difficult to quantify as species rely on a limited number of common resources. Investigating resource use at the bulk level may not always be of sufficient resolution to detect subtle differences in resource use, as species-specific nutritional niches at the biochemical level may also moderate diversity effects on resource use. Methodology/Principal Findings: Here we use three co-occurring marine benthic echinoderms (Brissopsis lyrifera, Mesothuria intestinalis, Parastichopus tremulus) that feed on the same phytodetrital food source, to determine whether resource partitioning is the principal mechanism underpinning diversity effects on resource use. Specifically we investigate the use of phytodetrital pigments ( chlorophylls and carotenoids) because many of these are essential for biological functions, including reproduction. Pigments were identified and quantified using reverse-phase high performance liquid Chromatography ( HPLC) and data were analysed using a combination of extended linear regression with generalised least squares (GLS) estimation and standard multivariate techniques. Our analyses reveal no species-specific selectivity for particular algal pigments, confirming that these three species do not partition food resources at the biochemical level. Nevertheless, we demonstrate increased total resource use in diverse treatments as a result of selection effects and the dominance of one species (B. lyrifera). Conclusion: Overall, we found no evidence for resource partitioning at the biochemical level, as pigment composition was similar between individuals, which is likely due to plentiful food availability. Reduced intra-specific competition in the species mixture combined with greater adsorption efficiency and differences in feeding behaviour likely explain the dominant use of resources by B. lyrifera

    T-helper 22 cells develop as a distinct lineage from Th17 cells during bacterial infection and phenotypic stability is regulated by T-bet.

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    CD4+ T-helper 22 (Th22) cells are a phenotypically distinct lymphocyte subset that produces high levels of interleukin (IL)-22 without co-production of IL-17A. However, the developmental origin and lineage classification of Th22 cells, their interrelationship to Th17 cells, and potential for plasticity at sites of infection and inflammation remain largely undefined. An improved understanding of the mechanisms underpinning the outgrowth of Th22 cells will provide insights into their regulation during homeostasis, infection, and disease. To address this knowledge gap we generated 'IL-17A-fate-mapping IL-17A/IL-22 reporter transgenic mice' and show that Th22 cells develop in the gastrointestinal tract and lung during bacterial infection without transitioning via an Il17a-expressing intermediate, although in some compartments alternative transition pathways exist. Th22-cell development was not dependent on T-bet; however, this transcription factor functioned as a promiscuous T-cell-intrinsic regulator of IL-17A and IL-22 production, in addition to regulating the outgrowth, phenotypic stability, and plasticity of Th22 cells. Thus, we demonstrate that at sites of mucosal bacterial infection Th22 cells develop as a distinct lineage independently of Th17 cells; though both lineages exhibit bidirectional phenotypic flexibility within infected tissues and their draining lymph nodes, and that T-bet plays a critical regulatory role in Th22-cell function and identity

    Comparison of the suppressive effects of soluble CR1 and C5a receptor antagonist in acute arthritis induced in rats by blocking of CD59

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    We investigated the effects of suppression of complement activation at C3 level and inhibition of C5a on acute synovitis in rats. Acute synovitis was induced in Wistar rats by intra-articular (i.a.) injection into one knee of 0.3 mg of MoAb 6D1 (anti-rat CD59 antibody). In the treatment groups, soluble CR1 (sCR1) or C5a receptor (C5aR) antagonist was administered intra-articularly or intravenously and effects on the course of the acute synovitis were monitored. Synovitis induced by 6D1 was characterized by joint swelling, thickening of synovial tissue, cellular infiltration and deposition of membrane attack complex (MAC) on the synovial surface. Neither inflammatory change nor MAC deposition was found in rats which received an i.a. injection of sCR1 to suppress complement activity in the joint. Intra-articular injection of sCR1 did not reduce plasma complement activity. Intravenous administration of sCR1 suppressed plasma complement activity but had no effect on the course of the arthritis and synovitis with MAC deposition was observed. Neither i.a. nor i.v. injection of C5aR antagonist had any suppressive effects on inflammatory change or MAC deposition in synovium. The data show that inflammatory change induced by 6D1 was mediated by local complement activation and was not accompanied by systemic complement activation. C5a generation was not responsible for the observed inflammation, suggesting that other complement activation products, possibly MAC, mediate the inflammatory change observed in this model of acute synovitis in rats
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