Abstract
Regulatory T cells (Tregs) suppress excessive immune responses and are potential therapeutic targets in autoimmune disease and organ transplantation rejection. However, their role in renal ischemia-reperfusion injury (IRI) is unclear. Levels of Tregs and expression of CXCR3 in Tregs were analyzed to investigate their function in the early phase of renal IRI. Mice were randomly divided into Sham, IRI, and anti-CD25 (PC61) + IRI groups. The PC61 + IRI group was established by i.p. injection of PC61 monoclonal antibody (mAb) to deplete Tregs before renal ischemia. CD4+CD25+Foxp3+ Tregs and CXCR3 on Tregs were analyzed by flow cytometry. Blood urea nitrogen (BUN), serum creatinine (Scr) levels, and tubular necrosis scores, all measures of kidney injury, were greater in the IRI group than in the Sham group. Numbers of Tregs were increased at 72 h after reperfusion in kidney. PC61 mAb preconditioning decreased the numbers of Tregs and aggravated kidney injury. There was no expression of CXCR3 on Tregs in normal kidney, while it expanded at 72 h after reperfusion and inversely correlated with BUN, Scr, and kidney histology score. This indicated that recruitment of Tregs into the kidney was related to the recovery of renal function after IRI and CXCR3 might be involved in the migration of Tregs.
Highlights
Ischemia-reperfusion injury (IRI) is a common and important clinical problem in many different organs
The Blood urea nitrogen (BUN) and serum creatinine (Scr) concentrations were decreased at 72 h compared with those at 24 h in the IRI group (P < 0.05), both concentrations were still greater than those in the Sham group (P < 0.05)
With PC61 monoclonal antibody (mAb) administration before renal ischemia, BUN and Scr levels were greater at 72 h (28.3±2.3 mmol/L versus 17.4± 2.8 mmol/L and 58.4 ± 7.2 μmol/L versus 38.6 ± 8.4 μmol/L, resp., P < 0.05) but not at 24 h after reperfusion as compared with the IRI group (Figure 1)
Summary
Ischemia-reperfusion injury (IRI) is a common and important clinical problem in many different organs. It has a critical role in the pathogenesis of acute renal failure and graft rejection, is associated with increased morbidity and mortality, and is closely related to the development of chronic kidney disease [1, 2]. There was a viewpoint that both T and B cells constituted the primary mediators of the adaptive immune response and did not play a role in the acute phase of IRI. Recent data have challenged this assumption and demonstrate an important modulatory role of T cells in IRI [6,7,8]
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