Journal ArticleDOI
The Fas Death Factor
Shigekazu Nagata,Pierre Golstein +1 more
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TLDR
Fas ligand (FasL), a cell surface molecule belonging to the tumor necrosis factor family, binds to its receptor Fas, thus inducing apoptosis of Fas-bearing cells.Abstract:
Fas ligand (FasL), a cell surface molecule belonging to the tumor necrosis factor family, binds to its receptor Fas, thus inducing apoptosis of Fas-bearing cells. Various cells express Fas, whereas FasL is expressed predominantly in activated T cells. In the immune system, Fas and FasL are involved in down-regulation of immune reactions as well as in T cell-mediated cytotoxicity. Malfunction of the Fas system causes lymphoproliferative disorders and accelerates autoimmune diseases, whereas its exacerbation may cause tissue destruction.read more
Citations
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CTLA-4-mediated inhibition in regulation of T cell responses: mechanisms and manipulation in tumor immunotherapy.
TL;DR: Newly emerging data suggest that inhibitory signals mediated by CTLA-4 not only can determine whether T cells become activated, but also can play a role in regulating the clonal representation in a polyclonal response.
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Caspase activation: the induced-proximity model.
Guy S. Salvesen,Vishva M. Dixit +1 more
TL;DR: Evidence for a hypothesis-the induced-proximity model-that describes how the first proteolytic signal is produced after adapter-mediated clustering of initiator caspase zymogens is reviewed.
Journal ArticleDOI
Apoptotic dna fragmentation
TL;DR: The molecular mechanism of and the physiological roles played by apoptotic DNA fragmentation will be discussed.
Journal ArticleDOI
The fas counterattack : fas-mediated T cell killing by colon cancer cells expressing fas ligand
TL;DR: A Fas counterattack model for immune escape in colon cancer is suggested, whereby the cancer cells resist Fas-mediated T cell cytotoxicity but express functional FasL, an apoptotic death signal to which activated T cells are inherently sensitive.
Journal ArticleDOI
Targeting apoptosis in cancer therapy
TL;DR: The main pathways that regulate apoptosis as well as other signalling pathways that interact with them are presented, highlighting actionable molecular targets for anticancer therapy and an overview of therapeutic agents exploiting apoptosis currently in clinical translation and known mechanisms of resistance to these agents are provided.
References
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Journal ArticleDOI
Lymphoproliferation disorder in mice explained by defects in Fas antigen that mediates apoptosis
Rie Watanabe-Fukunaga,Camilynn I. Brannan,Neal G. Copeland,Nancy A. Jenkins,Shigekazu Nagata +4 more
TL;DR: The Ipr mice develop lymphadenopathy and suffer from a systemic lupus erythematosus-like autoimmune disease, indicating an important role for Fas antigen in the negative selection of autoreactive T cells in the thymus.
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The polypeptide encoded by the cDNA for human cell surface antigen Fas can mediate apoptosis.
Naoto Itoh,Shin Yonehara,Ai Ishii,Minako Yonehara,Sei Ichi Mizushima,Masazumi Sameshima,Atsushi Hase,Yoshiyuki Seto,Shigekazu Nagata +8 more
TL;DR: Complementary DNAs encoding the cell surface antigen Fas were isolated from a cDNA library of human T cell lymphoma KT-3 cells and revealed that the molecule coding for the Fas antigen determinant is a 319 amino acid polypeptide with a single transmembrane domain.
Journal ArticleDOI
Social controls on cell survival and cell death
TL;DR: For some mammalian cells, programmed death seems to occur by default unless suppressed by signals from other cells, so dependence on specific survival signals provides a simple way to eliminate misplaced cells, for regulating cell numbers and, perhaps, for selecting the fittest cells.
Journal ArticleDOI
Molecular cloning and expression of the fas ligand, a novel member of the tumor necrosis factor family
TL;DR: Northern hybridization revealed that Fas ligand is expressed in activated splenocytes and thymocytes, consistent with its involvement in T cell-mediated cytotoxicity and in several nonlymphoid tissues, such as testis.
Journal ArticleDOI
Site-restricted persistent cytomegalovirus infection after selective long-term depletion of CD4+ T lymphocytes.
TL;DR: The CD8+ effector cells raised in the CD4 subset- deficient host were able of clear vital tissues from productive infection and to restrict asymptomatic, persistent infection to acinar glandular epithelial cells in salivary gland tissue.