IL-17 producing CD4+ T cells mediate accelerated ischemia/reperfusion-induced injury in autoimmunity-prone mice.
IL-17 producing CD4+ T cells mediate accelerated ischemia/reperfusion-induced injury in autoimmunity-prone mice.
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DOI：
10.1016/j.clim.2008.09.019
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发表时间：
2009-03
期刊：
影响因子：
--
通讯作者：
Tsokos GC
中科院分区：
文献类型：
--
作者：
Edgerton C;Crispín JC;Moratz CM;Bettelli E;Oukka M;Simovic M;Zacharia A;Egan R;Chen J;Dalle Lucca JJ;Juang YT;Tsokos GC
先天性和适应性免疫反应的要素与缺血再灌注（I/R）后的组织损伤发展有关。在此我们证明，在再灌注的第一个小时内，T细胞会浸润经历肠道I/R的C57BL/6小鼠的肠道。在经历肠道I/R的B6.MRL/lpr小鼠中，T细胞浸润的强度更高，并且反映出比对照小鼠更严重的组织损伤。T细胞的耗竭限制了B6.MRL/lpr小鼠的I/R损伤，而将B6.MRL/lpr淋巴结来源的T细胞回输到对I/R有抵抗力的Rag - 1 - / -小鼠体内则重建了组织损伤。发现浸润组织的T细胞会产生白细胞介素 - 17。最后，已知不能产生白细胞介素 - 17的白细胞介素 - 23缺陷小鼠在经历I/R时肠道损伤明显较轻。我们的数据表明，T细胞通过产生促炎细胞因子白细胞介素 - 17在肠道I/R损伤中起主要作用。
Elements of the innate and adaptive immune response have been implicated in the development of tissue damage after ischemic reperfusion (I/R). Here we demonstrate that T cells infiltrate the intestine of C57BL/6 mice subjected to intestinal I/R during the first hour of reperfusion. The intensity of the T cell infiltration was higher in B6.MRL/lpr mice subjected to intestinal I/R and reflected more severe tissue damage than that observed in control mice. Depletion of T cells limited I/R damage in B6.MRL/lpr mice, whereas repletion of B6.MRL/lpr lymph node-derived T cells into the I/R-resistant Rag-1-/- mouse reconstituted tissue injury. The tissue-infiltrating T cells were found to produce IL-17. Finally, IL-23 deficient mice, which are known not to produce IL-17, displayed significantly less intestinal damage when subjected to I/R. Our data assign T cells a major role in intestinal I/R damage by virtue of producing the pro-inflammatory cytokine IL-17.
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