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T cells in renal ischemia-reperfusion injury1Clinical 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
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,
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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
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T cells into the kidney was reduced in
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T cell-deficient mice until 72 h after ischemia. In contrast,
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T cell infiltration was equal in wild-type and
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T cell-deficient mice, suggesting an interaction between
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and
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T cells. Data from
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T cell-deficient mice were confirmed by in vivo depletion of
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T cells in C57BL/6 mice. Whereas
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T cell-deficient mice were still protected after 120 h,
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T cell-deficient mice showed a "delayed wild-type phenotype" with a dramatic increase in kidney-infiltrating
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, Tcr-expressing CD4+ T-cells. This report provides further evidence that
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T cells are major effector cells in renal IRI, whereas
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T cells play a role as mediator cells in the first 72 h of renal IRI.
inflammation; acute renal failure
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