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首页> 外文期刊>Scandinavian journal of immunology. >Proliferative effect of dextran sulfate sodium (DSS)-pulsed macrophages on T cells from mice with DSS-induced colitis and inhibition of effect by IgG.
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Proliferative effect of dextran sulfate sodium (DSS)-pulsed macrophages on T cells from mice with DSS-induced colitis and inhibition of effect by IgG.

机译:硫酸葡聚糖硫酸钠(DSS)刺激的巨噬细胞对DSS诱导的结肠炎小鼠T细胞的增殖作用以及IgG的抑制作用。

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摘要

The authors have previously reported that homologous immunoglobulin (Ig)G reduces the occurrence of dextran sulfate sodium (DSS)-induced colitis, mainly by suppressing recruitment of immunocompetent cells into colitis lesions. However, the mechanisms of cell recruitment and of its suppression by IgG remain unclear. In addressing these questions, this study focused on the activation of T cells in the presence of macrophages. The authors found that [3H]-thymidine uptake of T cells from DSS-induced colitis mice, but not from normal mice, was significantly enhanced when cultured with DSS-pulsed macrophages. From the profile of cytokine production, it was suggested that T helper 1 (Th1)-type cells become predominant during stimulation. Addition of homologous IgG significantly suppressed T cell proliferation in a dose-dependent manner, while no suppressive effect was observed with heterologous IgG. Mouse IgG F(ab')2, but not Fc, fragments partially mimicked the suppressive effect of whole IgG. These findingsprovide evidence that Th1-type cells may play an important role in the development of DSS-induced colitis and that homologous IgG exerts its protective action at least in part through the F(ab')2 portion.
机译:作者先前曾报道过,同源免疫球蛋白(Ig)G可以减少葡聚糖硫酸钠(DSS)诱导的结肠炎的发生,这主要是通过抑制免疫活性细胞募集到结肠炎病变中来实现的。然而,细胞募集及其被IgG抑制的机制仍不清楚。在解决这些问题时,本研究集中于巨噬细胞存在下的T细胞活化。作者发现,与DSS刺激的巨噬细胞一起培养时,DSS诱导的结肠炎小鼠而非正常小鼠的T细胞对[3H]-胸苷的摄取显着增强。从细胞因子产生的概况来看,提示T辅助1(Th1)型细胞在刺激过程中占主导地位。同源IgG的添加以剂量依赖性方式显着抑制T细胞增殖,而异源IgG没有观察到抑制作用。小鼠IgG F(ab')2(而非Fc)片段部分模仿了完整IgG的抑制作用。这些发现提供了证据,表明Th1型细胞可能在DSS诱导的结肠炎的发展中起重要作用,并且同源IgG至少部分地通过F(ab')2部分发挥其保护作用。

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