Cited by 968Cell death mechanisms and regulationT-cell and B-cell ImmunologyNF-κB Signaling Pathways

The many roles of FAS receptor signaling in the immune system

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Strasser, Andreas, Jost, Philipp J., Nagata, Shigekazu·2009·Immunity

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.

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Crossref · 10.1016/j.immuni.2009.01.001

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Research works printed but not linked: 2

  1. Fiedler P Schaetzlein CE Eibel H 1998 Constitutive expression of Fas ligand in thyrocytes Science 279 http://www.sciencemag.org/content/vol279/issue5359/
  2. Stokes TA Rymaszewski M Arscott PL Wang SH Bretz JD Bartron J Baker JRJ 1998 Constitutive expression of Fas ligand in thyrocytes Science 279 http://www.sciencemag.org/content/vol279/issue5359/

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Authors
Strasser, A., Jost, P. J., & Nagata, S.
Affiliations
  • Walter and Eliza Hall Institute of Medical Research (AU)
  • Kyoto University (JP)
Corresponding author
  • Strasser, Andreas
  • Nagata, Shigekazu
Venue
Immunity
Publisher
Elsevier BV
Published
2009-02
Volume
30
Issue
2
Pages
180-192
ISSN
1074-7613 (ISSN-L)
OpenAlex
W2016345107
Cited by
968
References
181
Citations by year
2026: 36 · 2025: 50 · 2024: 39 · 2023: 52 · 2022: 45 · 2021: 49 · 2020: 42 · 2019: 48 · 2018: 49 · 2017: 50 · 2016: 56 · 2015: 53 · 2014: 62 · 2013: 86 · 2012: 68
FWCI
6.37
Type
journal article
Language
en
Open access
Locations
  • Immunity (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Health and Medical Research Council
  • National Medical Research Council
  • National Cancer Institute (#CA 80188, R01CA043540, CA 43540, R01CA080188)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
Keywords
Fas, Fas ligand, TNF receptor superfamily, apoptosis signaling, FADD, caspase-8, Bid, Bcl-2 family proteins, autoimmunity, tumor suppression, lymphocyte death, hepatocytes
MeSH terms
Animals, Homeostasis, Humans, Immune System, Signal Transduction, Apoptosis, fas Receptor, Fas Ligand Protein

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