New kids in the block: the role of FasL and Fas in kidney damage

J Nephrol. May-Jun 1999;12(3):150-8.

Abstract

Fas ligand (FasL) is a lethal cytokine that promotes apoptosis through cross-linking of the Fas receptor, although it also has other, less well understood functions. The FasL/Fas system regulates immune and inflammatory responses. Evidence that FasL and Fas participate in kidney damage can be summarized as follows: 1) FasL is expressed by renal cells and its expression increases during kidney damage; 2) activation of the Fas receptor promotes apoptosis of non-stimulated or cytokine-primed renal cells in culture; 3) Fas agonists kill mesangial cells and induce glomerular injury in vivo, but can also reduce kidney damage by limiting injurious immunological responses; 4) mice with disrupted FasL/Fas systems are protected from acute tubular cell injury, although they develop autoimmune glomerulonephritis if other genetic predisposing factors are present. These facts imply that the FasL/Fas system can be considered a new target for therapeutic intervention in kidney damage. However, any therapeutic approach must consider interference with Fas in other cell systems. The complexities of the FasL/Fas system in the kidney are still far from clear.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Apoptosis / physiology*
  • Fas Ligand Protein
  • Kidney / pathology*
  • Ligands
  • Membrane Glycoproteins / physiology*
  • Mice
  • fas Receptor / physiology*

Substances

  • Fas Ligand Protein
  • Fasl protein, mouse
  • Ligands
  • Membrane Glycoproteins
  • fas Receptor