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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

A homozygous Fas ligand gene mutation in a patient causes a new type of autoimmune lymphoproliferative syndrome

TL;DR: Findings provide evidence that inherited nonlethal FASL abnormalities cause an uncommon apoptosis defect producing lymphoproliferative disease, and highlight the need for a review of the current ALPS classification to include a new ALPS type Ic subgroup.
Journal ArticleDOI

T Cells in Fish.

TL;DR: Recent progress in T cell research focusing on the tissue distribution and function of fish T cells is summarized.
Journal ArticleDOI

IFN-gamma action on pancreatic beta cells causes class I MHC upregulation but not diabetes.

TL;DR: This study dissociates class I MHC upregulation from progression to diabetes, shows that the rise in class II MHC is due to local IFN-gamma action, and eliminates beta cells as the targets of IFN in autoimmune diabetes.
Journal ArticleDOI

Cellular and Molecular Mechanisms of Parkinson’s Disease: Neurotoxins, Causative Genes, and Inflammatory Cytokines

TL;DR: Accumulating evidences points to a hypothesis that multiple primary causes of PD may be ultimately linked to a final common signal-transduction pathway leading to programmed cell death, i.e., apoptosis or autophagy, of the CA neurons.
Journal ArticleDOI

Molecular regulation of cell-cycle progression and apoptosis in mammalian cells: implications for biotechnology.

TL;DR: This review summarizes the genes, proteins, and interactions presently known to control apoptosis and cell‐cycle progression and access to the component genes and proteins have already been applied to guide research and development in bioprocess technology and medical treatment.
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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