Expression and function of Fas during differentiation and activation of B cells

Int Rev Immunol. 1999;18(4):367-79. doi: 10.3109/08830189909088489.


Fas (Apo-1, CD95) cell surface antigen belongs to the tumor necrosis factor receptor family and mediates apoptosis of a variety of cell types, including lymphocytes, after ligation with Fas ligand (FasL). Recent studies on the role of Fas/FasL interaction in the immune responses strongly suggest the relevance of dysregulation in Fas-mediated apoptosis as a cause of autoimmune disorders. While Fas is not an essential molecule in the elimination or functional inactivation (anergy) of autoreactive B cells, it is indispensable to the maintenance of peripheral tolerance and prevention of autoimmunity. Studies in the past few years have begun to reveal the mechanism by which susceptibility to Fas-mediated apoptosis in B cells is regulated to allow antigen-specific B cells survive and differentiate and to eliminate nonspecifically activated, potentially selfreactive B cells.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis
  • Autoimmunity
  • B-Lymphocytes / physiology*
  • CD40 Ligand
  • Cell Differentiation
  • Humans
  • Interleukin-4 / physiology
  • Lymphocyte Activation*
  • Membrane Glycoproteins / physiology
  • Receptors, Antigen, B-Cell / physiology
  • fas Receptor / physiology*


  • Membrane Glycoproteins
  • Receptors, Antigen, B-Cell
  • fas Receptor
  • CD40 Ligand
  • Interleukin-4