Journal
TRANSPLANT IMMUNOLOGY
Volume 22, Issue 1-2, Pages 44-54Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.trim.2009.08.001
Keywords
Ischemia-reperfusion injury; Anti-thymocyte globulin; Immune mechanisms
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Funding
- Genzyme Corp
- US National Institutes of Health
- US National Kidney Foundation
- Talecris Biotech.Inc
- Korea Research Foundation
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Kidney ischemia-reperfusion injury (IRI) is an important contributor to delayed graft function (DGF) and poor outcome of allografts. Small clinical studies suggest a beneficial role for human anti-thymocyte globulin (ATG) in DGF. We investigated the short-term effect of mouse anti-thymocyte globulin (mATG) on kidney warm IRI in mice. We administered either mATG, rabbit immunoglobulin (RIgG), or saline with different dosing schedules in three different IRI models: 30 min bilateral, 60 min bilateral, and 45 min unilateral IRI. mATG effectively depleted circulating T cells but had less effect on kidney-infiltrating T cells. There was no difference in serum creatinine levels between groups in each study. Scoring of renal tubular damage and regenerating tubules revealed no difference between groups. The percentage of CD3(+)CD4(-)CD8(-) double-negative (DN) T cells, which were reported to contribute to the pathogenesis of lupus nephritis, increased and the percentages of regulatory T cells and NK cells decreased in the post-ischemic kidneys of mATG treated mice. mATG did not alter the expression of pro-inflammatory cytokines such as IFN-gamma or anti-inflammatory cytokines such as IL-10 in post-ischemic kidneys. mATG treatment, whether initiated before ischemia or immediately after reperfusion, had minimal effects on renal injury following warm IRI in mice. (C) 2009 Elsevier B.V. All rights reserved.
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