Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8463865 | Cellular Immunology | 2014 | 6 Pages |
Abstract
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 72Â 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 72Â h after reperfusion. Depletion of CD4+CD25highCD127low Tregs was associated with worsening of renal function and histology, particularly at 72Â 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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Authors
Jun Cao, Ke Wei, Qingshu Li, Ping Li, Jun Dong, Jie Luo, Bo Cheng, Su Min,