B cells in systemic autoimmune disease: recent insights from Fas-deficient mice and men

Curr Opin Immunol. 1996 Dec;8(6):852-9. doi: 10.1016/s0952-7915(96)80015-x.

Abstract

In mice functionally deficient for either Fas or Fas ligand expression, the failure of Fas-ligand-expressing cytotoxic T cells to eliminate autoreactive B cells can result in excessive autoantibody production. Recent in vitro studies have shown that B cells activated by CD40 ligand become extremely sensitive to Fas-mediated apoptosis while IL-4 and/or surface IgM receptor engagement protects B cells from Fas ligand cytolysis. Potential in vivo sites for Fas ligand regulation of self-reactive B cells have been suggested and implications for human disease have been investigated.

Publication types

  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Autoimmune Diseases / genetics*
  • Autoimmune Diseases / immunology
  • Fas Ligand Protein
  • Humans
  • Ligands
  • Membrane Glycoproteins / genetics
  • Mice
  • Mice, Mutant Strains
  • fas Receptor / genetics*

Substances

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