白细胞介素-7受体
白细胞介素2受体
发病机制
肾
肾缺血
医学
肾功能
缺血
免疫学
免疫系统
内科学
再灌注损伤
T细胞
作者
Cao Jun,Wei Ke,Li Qingshu,Li Ping,Dong Jun,Luo Jie,Cheng Bo,Min Su
标识
DOI:10.1016/j.cellimm.2014.04.002
摘要
Ischemia reperfusion injury (IRI) is critical in the pathogenesis of acute renal failure and graft rejection. Regulatory T cells (Tregs) suppress excessive immune responses in IRI. We investigated the role of CD4+CD25highCD127low Tregs in the early phase of renal IRI pathogenesis in a mouse model. CD4+CD25highCD127low Tregs in the kidney, tubular necrosis scores, and renal function were measured 24 or 72 h after reperfusion. PC61, an anti-CD25 monoclonal antibody, was used to deplete Tregs before renal ischemia to confirm the effect of these Tregs. CD4+CD25highCD127low Tregs were expanded 24 and 72 h after reperfusion. Depletion of CD4+CD25highCD127low Tregs was associated with worsening of renal function and histology, particularly at 72 h after reperfusion. These results indicated that expansion of CD4+CD25highCD127low Tregs in the early phase of renal IRI may participate in tissue repair. These data reveal new insights into the pathogenesis of ischemic acute renal failure and a novel therapeutic approach.
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