Author/Authors :
Jun، نويسنده , , Cao and Ke، نويسنده , , Wei and Qingshu، نويسنده , , Li and Ping، نويسنده , , Li and Jun، نويسنده , , Dong and Jie، نويسنده , , Luo and Bo، نويسنده , , Cheng and Su، نويسنده , , Min، نويسنده ,
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 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.
Keywords :
Renal Insufficiency , Ischemia , T-lymphocytes , Regulatory