Journal
CELLULAR IMMUNOLOGY
Volume 289, Issue 1-2, Pages 106-111Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.cellimm.2014.04.002
Keywords
Ischemia; T-lymphocytes; Regulatory; Renal insufficiency
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Funding
- Chinese national clinical construction specialty
- Chongqing medical construction specialty
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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(+) CD25(high)CD127(low) Tregs in the early phase of renal IRI pathogenesis in a mouse model. CD4(+)CD25(high) CD127(low) 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(+)CD25highCD127(low) Tregs were expanded 24 and 72 h after reperfusion. Depletion of CD4(+)CD25(high)CD127(low) Tregs was associated with worsening of renal function and histology, particularly at 72 h after reperfusion. These results indicated that expansion of CD4(+)CD25(high) CD127(low) 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. (C) 2014 Elsevier Inc. All rights reserved.
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