肾脏缺血再灌注损伤的免疫学机制研究进展

固有免疫和适应性免疫参与肾脏缺血再灌注损伤(ischemia-reperfusion injury,IRI).在IRI急性期,肾血管内皮细胞黏附分子表达和血管通透性增加；肾小管上皮细胞补体C3沉积和Toll样受体2、4表达增加；树突状细胞早期活化导致中性粒细胞、巨噬细胞、自然杀伤细胞、CD4+T细胞和B细胞等迁移到缺血后肾脏.可溶性免疫分子(如补体活化产物、细胞因子和趋化因子)参与肾脏IRI急性损伤和(或)修复.Foxp3+调节性T细胞和旁路活化的巨噬细胞参与肾脏IRI修复；而B细胞限制IRI修复.

Progress in immune mechanism of kidney ischemia-reperfusion injury

Both innate and adaptive immunity contribute to the pathogenesis of ischemia-reperfusion injury (IRI).During acute phase of kidney IRI,kidney endothelial cells promote inflammation after IRI by increasing adhesion molecule expression and vascular permeability,and tubular epithelial cells increase complement C3 binding and Toll-like receptor 2 and Toll-like receptor 4 expression.Early activation of kidney dendritic cells initiates a cascade of events leading to accumulation of neutrophils,macrophage,natural killer cells,CD4 + T cells and B cells in the early phase of renal IRI.Soluble components of the immune system,such as complement activation production,cytokines and chemokines,also are implicated in the injury and repair of post-ischemic kidneys.Foxp3 + regulatory T cells and alternatively activated macrophage participate in attenuating the inflammation and initiating the repair of kidney IRI,while B lymphocytes limit repair of kidney IRI.