Cell death induced by the Fas/Fas ligand pathway and its role in pathology

Immunol Cell Biol. 1999 Aug;77(4):312-7. doi: 10.1046/j.1440-1711.1999.00837.x.


Engagement of the cell death surface receptor Fas by Fas ligand (FasL) results in apoptotic cell death, mediated by caspase activation. Cell death mediated via Fas/FasL interaction is important for homeostasis of cells in the immune system and for maintaining immune-privileged sites in the body. Killing via the Fas/FasL pathway also constitutes an important pathway of killing for cytotoxic T cells. Fas ligand is induced in activated T cells, resulting in activation-induced cell death by the Fas/FasL pathway. Recently it has been shown that the Fas receptor can also be up-regulated following a lesion to the cell, particularly that induced by DNA-damaging agents. This can then result in killing of the cell by a Fas/FasL-dependent pathway. Up-regulation of Fas receptor following DNA damage appears to be p53 dependent.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis / immunology*
  • Apoptosis / physiology
  • DNA Damage
  • Fas Ligand Protein
  • Humans
  • Ligands
  • Lymphocyte Activation
  • Membrane Glycoproteins / physiology*
  • T-Lymphocytes / cytology
  • T-Lymphocytes / immunology
  • T-Lymphocytes, Cytotoxic / immunology
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / physiology
  • Up-Regulation
  • fas Receptor / physiology*


  • FASLG protein, human
  • Fas Ligand Protein
  • Ligands
  • Membrane Glycoproteins
  • Tumor Suppressor Protein p53
  • fas Receptor