Expression and function of Fas during differentiation and activation of B cells.
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.
Wang
J
J
Department of Molecular Immunology, Kyushu University, Fukuoka, Japan.
Watanabe
T
T
D000818:Animals; D017209:Apoptosis; D015551:Autoimmunity; D001402:B-Lymphocytes / Q000502:physiology*; D023201:CD40 Ligand; D002454:Cell Differentiation; D006801:Humans; D015847:Interleukin-4 / Q000502:physiology; D008213:Lymphocyte Activation; D008562:Membrane Glycoproteins / Q000502:physiology; D011947:Receptors, Antigen, B-Cell / Q000502:physiology; D019014:fas Receptor / Q000502:physiology*
D008562:Membrane Glycoproteins; D011947:Receptors, Antigen, B-Cell; D019014:fas Receptor; D023201:CD40 Ligand; D015847:Interleukin-4