The effect of murine anti-thymocyte globulin on experimental kidney warm ischemia-reperfusion injury in mice
- Authors
- Jang H.R.; Gandolfo M.T.; Ko G.J.; Racusen L.; Rabb H.
- Issue Date
- 2009
- Keywords
- Anti-thymocyte globulin; Immune mechanisms; Ischemia-reperfusion injury
- Citation
- Transplant Immunology, v.22, no.1-2, pp 44 - 54
- Pages
- 11
- Indexed
- SCOPUS
- Journal Title
- Transplant Immunology
- Volume
- 22
- Number
- 1-2
- Start Page
- 44
- End Page
- 54
- URI
- https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/16552
- DOI
- 10.1016/j.trim.2009.08.001
- ISSN
- 0966-3274
1878-5492
- Abstract
- 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-γ 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. © 2009 Elsevier B.V. All rights reserved.
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- Appears in
Collections - 2. Clinical Science > Department of Nephrology and Hypertension > 1. Journal Articles
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