title: The effect of murine anti-thymocyte globulin on experimental kidney warm ischemia-reperfusion injury in mice.
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 45min 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.
authors.affiliation: Nephrology Division, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. shinehr@gmail.com
authors.forename: Hye Ryoun
authors.initials: HR
authors.lastname: Jang
authors.forename: Maria Teresa
authors.initials: MT
authors.lastname: Gandolfo
authors.forename: Gang Jee
authors.initials: GJ
authors.lastname: Ko
authors.forename: Lorraine
authors.initials: L
authors.lastname: Racusen
authors.forename: Hamid
authors.initials: H
authors.lastname: Rabb
mesh_terms: D000818:Animals; D000961:Antilymphocyte Serum / Q000627:therapeutic use*; D001772:Blood Cell Count; D018925:Chemokines / Q000378:metabolism; D003404:Creatinine / Q000097:blood; D016207:Cytokines / Q000378:metabolism; D007074:Immunoglobulin G / Q000627:therapeutic use; D007668:Kidney / Q000098:blood supply / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D007672:Kidney Cortex / Q000473:pathology; D007679:Kidney Medulla / Q000473:pathology; D007684:Kidney Tubules / Q000473:pathology; D008212:Lymphocyte Depletion; D016131:Lymphocyte Subsets / Q000166:cytology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D011817:Rabbits; D015427:Reperfusion Injury / Q000276:immunology / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D013154:Spleen / Q000473:pathology; D015996:Survival Rate; D013601:T-Lymphocytes / Q000166:cytology / Q000276:immunology
chemical_list: D000961:Antilymphocyte Serum; D018925:Chemokines; D016207:Cytokines; D007074:Immunoglobulin G; D003404:Creatinine