Contribution of CD4+ T cells to the early mechanisms of ischemia- reperfusion injury in a mouse model of acute renal failure

Contribution of CD4+ T cells to the early mechanisms of ischemia- reperfusion injury in a mouse model of acute renal failure

Autor Pinheiro, Helady Sanders Autor UNIFESP Google Scholar
Câmara, Niels Olsen Saraiva Autor UNIFESP Google Scholar
Noronha, Irene Lourdes Google Scholar
Longo-Maugéri, Ieda Maria Autor UNIFESP Google Scholar
Franco, Marcello Fabiano de Autor UNIFESP Google Scholar
Medina, J.o.a.p. Autor UNIFESP Google Scholar
Pacheco-Silva, Alvaro Autor UNIFESP Google Scholar
Instituição Universidade Federal de São Paulo (UNIFESP)
Universidade Federal de Juiz de Fora Divisão de Nefrologia
Universidade de São Paulo (USP)
Resumo Renal ischemia-reperfusion (IR) injury is the major cause of acute renal failure in native and transplanted kidneys. Mononuclear leukocytes have been reported in renal tissue as part of the innate and adaptive responses triggered by IR. We investigated the participation of CD4+ T lymphocytes in the pathogenesis of renal IR injury. Male mice (C57BL/6, 8 to 12 weeks old) were submitted to 45 min of ischemia by renal pedicle clamping followed by reperfusion. We evaluated the role of CD4+ T cells using a monoclonal depleting antibody against CD4 (GK1.5, 50 µ, ip), and class II-major histocompatibility complex molecule knockout mice. Both CD4-depleted groups showed a marked improvement in renal function compared to the ischemic group, despite the fact that GK1.5 mAb treatment promoted a profound CD4 depletion (to less than 5% compared to normal controls) only within the first 24 h after IR. CD4-depleted groups presented a significant improvement in 5-day survival (84 vs 80 vs 39%; antibody treated, knockout mice and non-depleted groups, respectively) and also a significant reduction in the tubular necrosis area with an early tubular regeneration pattern. The peak of CD4-positive cell infiltration occurred on day 2, coinciding with the high expression of ßC mRNA and increased urea levels. CD4 depletion did not alter the CD11b infiltrate or the IFN-g and granzyme-B mRNA expression in renal tissue. These data indicate that a CD4+ subset of T lymphocytes may be implicated as key mediators of very early inflammatory responses after renal IR injury and that targeting CD4+ T lymphocytes may yield novel therapies.
Palavra-chave Ischemia-reperfusion
Kidney inflammation
Leukocytes
CD4+ T lymphocytes
Kidney transplantation
Acute renal failure
Idioma Inglês
Data de publicação 2007-04-01
Publicado em Brazilian Journal of Medical and Biological Research. Associação Brasileira de Divulgação Científica, v. 40, n. 4, p. 557-568, 2007.
ISSN 0100-879X (Sherpa/Romeo, fator de impacto)
Publicador Associação Brasileira de Divulgação Científica
Extensão 557-568
Fonte http://dx.doi.org/10.1590/S0100-879X2007000400015
Direito de acesso Acesso aberto Open Access
Tipo Artigo
Web of Science WOS:000245440000015
SciELO S0100-879X2007000400015 (estatísticas na SciELO)
Endereço permanente http://repositorio.unifesp.br/handle/11600/3662

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