B cells in systemic autoimmune disease: recent insights from Fas-deficient mice and men.
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.
Elkon
K B
KB
Hospital for Special Surgery, Cornell University Medical Center, New York 10021, USA. ElkonK@hss.edu
Marshak-Rothstein
A
A
D000818:Animals; D001327:Autoimmune Diseases / Q000235:genetics* / Q000276:immunology; D053222:Fas Ligand Protein; D006801:Humans; D008024:Ligands; D008562:Membrane Glycoproteins / Q000235:genetics; D051379:Mice; D008817:Mice, Mutant Strains; D019014:fas Receptor / Q000235:genetics*
C505661:FASLG protein, human; D053222:Fas Ligand Protein; C505658:Fasl protein, mouse; D008024:Ligands; D008562:Membrane Glycoproteins; D019014:fas Receptor