Edgerton Colin, Crispín José C, Moratz Chantal M, Bettelli Estelle, Oukka Mohamed, Simovic Milomir, Zacharia Athina, Egan Ryan, Chen Jie, Dalle Lucca Jurandir J, Juang Yuang-Taung, Tsokos George C
Department of Medicine, Uniformed Services University for the Health Sciences, Bethesda, MD 20814, USA.
Clin Immunol. 2009 Mar;130(3):313-21. doi: 10.1016/j.clim.2008.09.019. Epub 2008 Dec 5.
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.
先天性和适应性免疫反应的成分与缺血再灌注（I/R）后组织损伤的发生有关。在此，我们证明在再灌注的第一个小时内，T细胞浸润了经历肠I/R的C57BL/6小鼠的肠道。在经历肠I/R的B6.MRL/lpr小鼠中，T细胞浸润的强度更高，并且与对照小鼠相比，反映出更严重的组织损伤。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细胞补充到抗I/R的Rag-1(-/-)小鼠中则重建了组织损伤。发现组织浸润性T细胞产生IL-17。最后，已知不产生IL-17的IL-23缺陷小鼠在经历I/R时表现出明显更少的肠道损伤。我们的数据表明，T细胞通过产生促炎细胞因子IL-17在肠I/R损伤中起主要作用。
