title: Contribution of T lymphocytes to rat renal ischemia/reperfusion injury.
abstract: BACKGROUND
  This study aimed to elucidate the early involvement of T lymphocytes in renal ischemia/reperfusion injury.
  
  
  METHODS
  Athymic nude rats (F344/N_Jcl-nu) and control F344/Jcl were subjected to 45 min unilateral renal ischemia. To determine whether the observed differences might be derived from the T lymphocyte presence, T lymphocytes from the spleens of F344/Jcl were injected into F344/N_Jcl-nu via tail vein at the initiation of reperfusion. Immunohistochemical analysis was performed for CD3, the proliferative cell nuclear antigen (PCNA), vimentin, and E-cadherin. T lymphocytes were obtained from the green fluorescent protein transgenic (GFP) rats, and transplanted to F344/N_Jcl-nu 10 min before reperfusion. The animals were euthanized 15 min after reperfusion.
  
  
  RESULTS
  F344/N_Jcl-nu showed less retention of both Cr and BUN at 24 and 48 h after reperfusion, compared with F344/Jcl. F344/N_Jcl-nu received T lymphocyte transplantation showed significantly higher retention of both Cr and BUN 24, 48, and 72 h after reperfusion than those without T lymphocyte. A rapid infiltration of T lymphocytes into proximal tubular epithelial cells and tubular lumen was observed using T lymphocytes with green fluorescent protein. In contrast, T lymphocytes were observed with much less frequency 24 h after ischemia. The number of PCNA-positive proximal tubular cells 24 h after the initiation of reperfusion was significantly smaller in the T lymphocyte transplantation group compared with the non-transplantation group. The vimentin positivity and cytoplasmic staining of E-cadherin were also more prominent in the transplantation group.
  
  
  CONCLUSIONS
  These findings demonstrate a rapid renal T lymphocyte infiltration, which propagate renal functional deterioration.
authors.affiliation: Department of Nephrology and Endocrinology 107 Lab, Hemodialysis and Apheresis, University Hospital, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, Japan. noiri-tky@umin.ac.jp
authors.forename: Eisei
authors.initials: E
authors.lastname: Noiri
authors.forename: Kent
authors.initials: K
authors.lastname: Doi
authors.forename: Reiko
authors.initials: R
authors.lastname: Inagi
authors.forename: Masaomi
authors.initials: M
authors.lastname: Nangaku
authors.forename: Toshiro
authors.initials: T
authors.lastname: Fujita
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified; D001806:Blood Urea Nitrogen; D017252:CD3 Complex / Q000378:metabolism; D015820:Cadherins / Q000378:metabolism; D002465:Cell Movement; D003404:Creatinine / Q000097:blood; D004195:Disease Models, Animal; D049452:Green Fluorescent Proteins / Q000235:genetics; D007150:Immunohistochemistry; D007668:Kidney / Q000098:blood supply* / Q000276:immunology*; D008297:Male; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D051381:Rats; D011916:Rats, Inbred F344; D011923:Rats, Nude; D015427:Reperfusion Injury / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology* / Q000637:transplantation; D013997:Time Factors; D014746:Vimentin / Q000378:metabolism
chemical_list: D017252:CD3 Complex; D015820:Cadherins; D018809:Proliferating Cell Nuclear Antigen; D014746:Vimentin; D049452:Green Fluorescent Proteins; D003404:Creatinine