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Journal ArticleDOI

The Fas Death Factor

Shigekazu Nagata, +1 more
- 10 Mar 1995 - 
- Vol. 267, Iss: 5203, pp 1449-1456
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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.

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Citations
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Journal ArticleDOI

Tyrosine Kinase-Dependent Activation of a Chloride Channel in CD95-Induced Apoptosis in T Lymphocytes

TL;DR: It is shown that CD95 receptor triggering activates an outwardly rectifying chloride channel (ORCC) in Jurkat T lymphocytes, and tyrosine kinase-mediated activation of ORCC may play a role in CD95-induced cell death in T lymphocyte.
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Challenges of Stem Cell Therapy for Spinal Cord Injury: Human Embryonic Stem Cells, Endogenous Neural Stem Cells, or Induced Pluripotent Stem Cells?

TL;DR: This review summarizes the pathophysiological mechanisms following SCI and compares human embryonic, adult neural, and the induced pluripotent stem cell‐based therapeutic strategies for SCI.
Journal ArticleDOI

Sphingomyelin breakdown and cell fate

TL;DR: A growing number of cell-surface receptors are now being shown to generate signals that trigger the hydrolysis of sphingomyelin to release diffusible ceramides, with outcomes as diverse as cell proliferation, differentiation, growth arrest and apoptosis.
Journal ArticleDOI

Fas-Mediated Apoptosis of CD4+ and CD8+ T Cells From Human Immunodeficiency Virus-Infected Persons: Differential In Vitro Preventive Effect of Cytokines and Protease Antagonists

TL;DR: It is reported here that CD4+ and CD8+ T cells from HIV-1-infected persons are sensitive to Fas (CD95/APO-1)-mediated death induced either by an agonistic anti-Fas antibody or by the physiologic soluble Fas ligand, although showing no sensitivity to tumor necrosis factor alpha-induced death.
References
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Journal ArticleDOI

Lymphoproliferation disorder in mice explained by defects in Fas antigen that mediates apoptosis

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.

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.
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