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Am J Physiol Renal Physiol 293: F741-F747, 2007. First published June 13, 2007; doi:10.1152/ajprenal.00486.2006
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Role of {alpha}/beta and {gamma}/{delta} T cells in renal ischemia-reperfusion injury

Kathrin Hochegger,1 Tobias Schätz,1 Philipp Eller,2 Andrea Tagwerker,1 Dorothea Heininger,1 Gert Mayer,1 and Alexander R. Rosenkranz1

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 {alpha}/beta, {gamma}/{delta} 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 {alpha}/beta T cells into the kidney was reduced in {gamma}/{delta} T cell-deficient mice until 72 h after ischemia. In contrast, {gamma}/{delta} T cell infiltration was equal in wild-type and {alpha}/beta T cell-deficient mice, suggesting an interaction between {alpha}/beta and {gamma}/{delta} T cells. Data from {gamma}/{delta} T cell-deficient mice were confirmed by in vivo depletion of {gamma}/{delta} T cells in C57BL/6 mice. Whereas {alpha}/beta T cell-deficient mice were still protected after 120 h, {gamma}/{delta} T cell-deficient mice showed a "delayed wild-type phenotype" with a dramatic increase in kidney-infiltrating {alpha}/beta, Tcr-expressing CD4+ T-cells. This report provides further evidence that {alpha}/beta T cells are major effector cells in renal IRI, whereas {gamma}/{delta} T cells play a role as mediator cells in the first 72 h of renal IRI.

inflammation; acute renal failure


Address for reprint requests and other correspondence: A. R. Rosenkranz, Clinical Div. of Nephrology, Clinical Dept. of Internal Medicine, Innsbruck Medical Univ., Anichstrasse 35, A-6020 Innsbruck, Austria (e-mail: alexander.rosenkranz{at}i-med.ac.at)






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