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Role of / and / T cells in renal ischemia-reperfusion injury

¹Clinical Division of Nephrology and ²Clinical Division of General Internal Medicine, Department of Internal Medicine, Innsbruck Medical University, Innsbruck, Austria

Submitted 11 December 2006 ; accepted in final form 11 June 2007

T cells have been implicated in the pathogenesis of renal ischemia-reperfusion injury (IRI). To date existing data about the role of the T cell receptor (Tcr) are contradictory. We hypothesize that the Tcr plays a prominent role in the late phase of renal IRI. Therefore, renal IRI was induced in /, / T cell-deficient and wild-type mice by clamping renal pedicles for 30 min and reperfusing for 24, 48, 72, and 120 h. Serum creatinine increased equally in all three groups 24 h after ischemia but significantly improved in Tcr-deficient animals compared with wild-type controls after 72 h. A significant reduction in renal tubular injury and infiltration of CD4⁺ T-cells in both Tcr-deficient mice compared with wild-type controls was detected. Infiltration of / T cells into the kidney was reduced in / T cell-deficient mice until 72 h after ischemia. In contrast, / T cell infiltration was equal in wild-type and / T cell-deficient mice, suggesting an interaction between / and / T cells. Data from / T cell-deficient mice were confirmed by in vivo depletion of / T cells in C57BL/6 mice. Whereas / T cell-deficient mice were still protected after 120 h, / T cell-deficient mice showed a "delayed wild-type phenotype" with a dramatic increase in kidney-infiltrating /, Tcr-expressing CD4⁺ T-cells. This report provides further evidence that / T cells are major effector cells in renal IRI, whereas / T cells play a role as mediator cells in the first 72 h of renal IRI.

inflammation; acute renal failure

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