aHospital for Special Surgery, Cornell University Medical Center, 535 East 70th Street, New York, NY 10021, USA;bDepartment of Microbiology, Boston University Medical School, 80 East Concord Street, Boston, MA 02118, USA
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.