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首页> 外文期刊>The Journal of Immunology: Official Journal of the American Association of Immunologists >Staphylococcal enterotoxin B stimulates expansion of autoreactive T cells that induce apoptosis in intestinal epithelial cells: regulation of autoreactive responses by IL-10.
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Staphylococcal enterotoxin B stimulates expansion of autoreactive T cells that induce apoptosis in intestinal epithelial cells: regulation of autoreactive responses by IL-10.

机译：葡萄球菌肠毒素B刺激自身反应性T细胞的扩增，从而诱导肠道上皮细胞凋亡：IL-10对自身反应性的调节。

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摘要

T cell responses to self Ags and normal microbial flora are carefully regulated to prevent autoreactivity. Because IL-10-deficient mice develop colitis, and this response is triggered by luminal flora, we investigated whether IL-10 regulates the ability of microbial Ags to induce autoreactive T cells that could contribute to intestinal inflammation. T cells from wild-type mice were primed with staphylococcal enterotoxin B (SEB) in vitro, which induced an autoreactive proliferative response to syngeneic feeder cells. The cells were predominately CD3+ and CD4+. T cells from IL-10-deficient mice were constitutively autoreactive, and SEB priming enhanced this further. The autoreactive, proliferative response of T cells from wild-type mice was suppressed by IL-10 in the primary or secondary culture, and this effect was inhibited by neutralizing Abs to the IL-10R. To confirm that an autoreactive repertoire was expanded after SEB priming, we used CBA/J mice (Mls-1a) in which autoreactive T cells recognizing the endogenous viral superantigen are depleted (Vbeta6, 7, 8.1 TCR-bearing cells). However, SEB rescued these autoreactive T cell repertoires. Adding anti-MHC class II Ab blocked the autoreactive response. SEB-primed splenic or colonic T cells also induced apoptosis in syngeneic intestinal epithelial cells that was blocked significantly by IL-10. Thus, microbial Ags have the potential to abrogate self tolerance by stimulating autoreactive T cells that become cytolytic to target cells. IL-10 plays a protective role in maintaining self tolerance after microbial stimulation by preventing the activation of T cells that contribute to epithelial cell damage.
机译：T细胞对自身Ag和正常微生物菌群的反应均经过仔细调节，以防止自身反应。由于缺乏IL-10的小鼠患上结肠炎，并且这种反应是由腔内菌群触发的，因此我们调查了IL-10是否调节微生物Ags诱导可能导致肠道炎症的自身反应性T细胞的能力。来自野生型小鼠的T细胞在体外用葡萄球菌肠毒素B（SEB）引发，这诱导了对同系饲养细胞的自身反应性增殖反应。细胞主要是CD3 +和CD4 +。来自IL-10缺陷小鼠的T细胞具有组成型自反应性，而SEB引发进一步增强了这一功能。在原代或继代培养物中，IL-10抑制了野生型小鼠T细胞的自身反应性增殖反应，并且通过将Abs中和到IL-10R抑制了该效应。为了确认SEB启动后自身反应性库得以扩展，我们使用了CBA / J小鼠（Mls-1a），其中识别内源性病毒超抗原的自身反应性T细胞被耗尽（Vbeta6、7、8.1 TCR轴承细胞）。但是，SEB挽救了这些自身反应性T细胞库。加入抗MHC II类抗体可阻止自身反应。 SEB引发的脾或结肠T细胞也诱导了同基因肠上皮细胞的凋亡，该凋亡被IL-10显着阻断。因此，微生物Ags有潜力通过刺激自身反应性T细胞（对靶细胞具有溶细胞作用）来消除自身耐受性。 IL-10在微生物刺激后通过防止T细胞活化而起自我保护作用，而T细胞活化可能导致上皮细胞受损。

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