The Many Roles of FAS Receptor Signaling in the Immune System
Details
Publication Year 2009-02-20,Volume 30,Issue #2,Page 180-192
Journal Title
IMMUNITY
Publication Type
Journal Article
Abstract
FAS belongs to the subgroup of the tumor necrosis factor receptor (TNF-R) family that contains an intracellular "death domain" and triggers apoptosis. Its physiological ligand FASL is a member of the TNF cytokine family. Studies with mutant mice and cells from human patients have shown that FAS plays critical roles in the immune system, including the killing of pathogen-infected cells and the death of obsolete and potentially dangerous lymphocytes. Fas thereby functions as a guardian against autoimmunity and tumor development. FAS triggers apoptosis through FADD-mediated recruitment and activation of caspase-8. In certain cells such as hepatocytes, albeit not lymphocytes, FAS-induced apoptosis requires amplification through proteolytic activation of the proapoptotic BCL-2 family member BID. Curiously, several components of the FAS signaling machinery have been implicated in nonapoptotic processes, including cellular activation, differentiation, and proliferation. This review describes current understanding of Fas-induced apoptosis signaling and proposes experimental strategies for future advances.
Publisher
CELL PRESS
Keywords
FAMILY-MEMBER BIM; AUTOIMMUNE LYMPHOPROLIFERATIVE SYNDROME; HEMATOPOIETIC PROGENITOR CELLS; DOMINANT INTERFERING MUTANT; BH3-ONLY PROTEIN BIM; MATURE T-LYMPHOCYTES; VERSUS-HOST-DISEASE; B-CELLS; INDUCED APOPTOSIS; BCL-2 FAMILY
Terms of Use/Rights Notice
Refer to copyright notice on published article.


Creation Date: 2009-02-20 12:00:00
An error has occurred. This application may no longer respond until reloaded. Reload 🗙