T cells as mediators in renal ischemia/reperfusion injury

Kidney Int. 2004 Aug;66(2):491-6. doi: 10.1111/j.1523-1755.2004.761_4.x.


Inflammation has been established to contribute substantially to the pathogenesis of ischemia/reperfusion (I/R) with a central role for particular cells, adhesion molecules, and cytokines. Until recently, most of the research trying to unravel the pathogenesis of I/R injury has been focused on the role of neutrophils. However, recent studies have brought evidence that T cells and macrophages are also important leukocyte mediators of renal and extrarenal (liver) I/R injury. In vivo depletion of CD4+ cells but not CD8+ cells in wild-type mice was protective in I/R of the kidney. A marked preservation of liver function was also found after I/R in T-cell deficient athymic mice. Blocking the b130/CD28 costimulatory pathway by CTLA-4 Ig (recombinant fusion protein) ameliorated renal dysfunction and decreased mononuclear cell infiltration in I/R of the kidney. b130-1 expression was found limited to the membrane of the endothelial cells of the ascending vasa recta, resulting in trapping of CD28-expressing CD4 T cells. This trapping of leukocytes results in the upstream congestion in the ascending arterial vasa recta, generating the since more than 150 years described medullary vascular congestion of the kidney soon after ischemic injury. It seems worthwhile to study a combination therapy using anti-inflammatory/anti-adhesion molecules in the early phase of I/R.

Publication types

  • Review

MeSH terms

  • Acute Kidney Injury / immunology*
  • Acute Kidney Injury / pathology
  • Acute Kidney Injury / physiopathology
  • Animals
  • Humans
  • Reperfusion Injury / immunology*
  • Reperfusion Injury / pathology
  • Reperfusion Injury / physiopathology
  • T-Lymphocytes / immunology*