Role of ¿/ß and ¿/¿ T cells in renal ischemia-reperfusion injury
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 α/β...
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Veröffentlicht in: | American journal of physiology. Renal physiology 2007-09, Vol.293 (3), p.F741 |
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Sprache: | eng |
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Zusammenfassung: | 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 α/β, ... 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 ... T-cells in both Tcr-deficient mice compared with wild-type controls was detected. Infiltration of α/β 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 α/β T cell-deficient mice, suggesting an interaction between α/β and ... T cells. Data from ... T cell-deficient mice were confirmed by in vivo depletion of ... T cells in C57BL/6 mice. Whereas α/β 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 α/β, Tcr-expressing ... T-cells. This report provides further evidence that α/β 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. (ProQuest: ... denotes formulae/symbols omitted.) |
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ISSN: | 1931-857X 1522-1466 |