The many roles of FAS receptor signaling in the immune system
By A. Strasser, P. Jost, S. Nagata. Immunity, 2009
966 citations recorded by the source corpus.
Summary FAS (also known as APO-1 or CD95) belongs to the subgroup of the tumor necrosis factor receptor (TNF-R) family that contain an intra-cellular ‘death domain’ and can trigger apoptosis. Its physiological ligand, FASL (CD95L), is a member of the corresponding TNF cytokine family. Studies with spontaneous mutant mice, gene-targeted mice and cells from human patients have shown that FAS and FASL play critical roles in the immune system, in particular in the killing of pathogen infected target cells and the death of no longer needed, potentially deleterious as well as autoreactive lymphocytes. This ligand-receptor pair thereby functions as a guardian against autoimmunity and tumor development. FASL-FAS signaling triggers apoptosis through FADD (Fas-associated protein with death domain, also called MORT1) adaptor protein-mediated recruitment and activation of the aspartate-specific cysteine protease, caspase-8. In certain cells such as hepatocytes, albeit not in lymphocytes, FAS-induced apoptosis signaling requires amplification through proteolytic activation of the pro-apoptotic BCL-2 family member BID. Curiously, several components of the FAS signaling machinery have been implicated in non-apoptotic processes, including cellular activation, differentiation and proliferation. Here we describe current knowledge of the roles of FASL and FAS in the immune system, discuss important unresolved issues and propose experimental approaches to address them.
Subfields: Cancer Research, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/d6e0989e7415d8bd9356b7604b5f33371af007cb
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Citations in the corpus
- Astrocytes: Key Regulators of Neuroinflammation. (2016, background): “Fas ligand (FasL) plays a major role in this process as it binds the death receptor Fas expressed by activated immune cells to induce programmed cell death via caspase signaling [87].”
- Overview of the Immune Response (2003, background): “Defects in Fas or in its ligand, FasL, result in autoimmune disorders with prominent lymphoproliferation.(108) Thus deregulated Fas or its ligand might contribute importantly to autoimmune diseases.”
- Murine Models of Systemic Lupus Erythematosus (2011, background): “Furthermore, a mutation on the FasL gene, termed generalized lymphoproliferative disease (gld), was shown to cause an autoimmune disorder similar to the lpr mutation [36, 37].”
- Programmed Cell Death in Animal Development and Disease (2011, neutral): “Caspase activation can also occur via association with death receptors, which leads to the oligomerization and activation of an initiator caspase, caspase-8 (Strasser et al., 2009).”
- How does p53 induce apoptosis and how does this relate to p53-mediated tumour suppression? (2017, background): “Conversely, the death receptor pathway activates apoptosis by recruitment and activation of the pro-form of caspase-8 via the adaptors FADD, and in some cases also TRADD, at the ligated death receptors at the plasma membrane.(44,45) In so-called type 1 cells (e.”