T cells in organ ischemia reperfusion injury.
T cells in organ ischemia reperfusion injury.
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DOI：
10.1097/mot.0000000000000064
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发表时间：
2014-04
影响因子：
2.2
通讯作者：
Zhai Y
中科院分区：
文献类型：
--
作者：
Rao J;Lu L;Zhai Y
缺血和再灌注损伤发生在多种临床环境中，并导致器官功能障碍/衰竭。尽管具有先天性炎性免疫性质，但T细胞在IRI的发病机制中起关键作用，其不仅包括CD 4 + T细胞，还包括CD 8+和γδ T细胞。这篇综述的重点是如何假定的Ag特异性T细胞参与的问题，其中包括他们是否在Ag依赖的方式发挥作用，他们如何发挥作用，细胞因子或共刺激分子介导的机制，以及是否不同的T细胞亚群，Th 1，Th 17，Treg，都参与并发挥独特的作用？特异性T细胞群，如效应记忆CD 4 T细胞，通过IR促进炎性免疫活化，而不依赖于它们的适应性，即，AG独立它们通过分泌细胞因子和表达共刺激分子来发挥作用，以促进或抑制先天免疫激活或促进组织修复/稳态，如分别由Th 1、Th 17或Th 2、Treg细胞所例示的。T细胞靶向治疗需要用策略来改进，以最大限度地消除T细胞的促炎性，但保留T细胞的抗炎/免疫调节特性，用于未来改善IRI的临床应用。
Ischemia and reperfusion injuries occur in multiple clinical settings and contribute to organ dysfunction/failures. Despite the innate inflammatory immune nature, T cells are critically involved in the pathogenesis of IRI, which includes not only CD4+ T cells, but also CD8+ and γδ T cells. This review focuses on questions of how putative Ag-specific T cells are involved, which include whether they function in Ag-dependent manner; how they function, cytokine- or costimulatory molecule-mediated mechanisms; and whether different T cell subsets, Th1, Th17, Treg, are all involved and play distinctive roles? Specific T cell populations, such as effector memory CD4 T cells, promote inflammatory immune activation by IR independent of their adaptive properties, i.e., Ag-independent. They function by secreting cytokines and expressing costimulatory molecules to either promote or inhibit innate immune activation or facilitate tissue repair/homeostasis, as exemplified by Th1, Th17 or Th2, Treg cells respectively. T cell targeted therapies need to be refined with strategies to maximally eliminate the pro-inflammatory but spare the anti-inflammatory/immune regulatory properties of T cells, for future clinical application to ameliorate IRI.