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首页> 外文期刊>Immunity >Oxazolone Colitis, a Th2 Colitis Model Resembling Ulcerative Colitis, Is Mediated by IL-13-Producing NK-T Cells.
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Oxazolone Colitis, a Th2 Colitis Model Resembling Ulcerative Colitis, Is Mediated by IL-13-Producing NK-T Cells.

机译:恶唑酮结肠炎是一种类似于溃疡性结肠炎的Th2结肠炎模型,由产生IL-13的NK-T细胞介导。

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摘要

Oxazolone colitis (OC) is an experimental colitis that has a histologic resemblance to human ulcerative colitis. Here we show that IL-13 production is a significant pathologic factor in OC since its neutralization by IL-13Ralpha2-Fc administration prevents colitis. We further show that OC is mediated by NK-T cells since it can be induced neither in mice depleted of NK-T cells nor in mice that cannot present antigen to NK-T cells and mice lacking an NK-T cell-associated TCR. Finally, we show that NK-T cells are the source of the IL-13, since they produce IL-13 upon stimulation by alpha-galactosylceramide, an NK-T cell-specific antigen. These data thus describe a cellular mechanism underlying an experimental colitis that may explain the pathogenesis of ulcerative colitis.
机译:恶唑酮结肠炎(OC)是一种实验性结肠炎,其组织学类似于人溃疡性结肠炎。在这里,我们显示IL-13的产生是OC中的重要病理因素,因为通过IL-13Ralpha2-Fc的中和可以预防结肠炎。我们进一步表明OC是由NK-T细胞介导的,因为它既不能在耗尽NK-T细胞的小鼠中诱导,也不能在不能向NK-T细胞呈递抗原的小鼠中诱导,也不能在缺乏NK-T细胞相关TCR的小鼠中诱导。最后,我们显示NK-T细胞是IL-13的来源,因为它们在受到α-半乳糖神经酰胺(一种NK-T细胞特异性抗原)刺激后会产生IL-13。因此,这些数据描述了实验性结肠炎的基础细胞机制,可以解释溃疡性结肠炎的发病机理。

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