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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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Monoclonal antibody therapeutics and apoptosis

TL;DR: This review will focus on the mechanisms by which antibodies are capable of eliciting programmed cell death either directly or indirectly within tumor cells.
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Regulation of apo-2 ligand/trail expression in nk cells—involvement in nk cell-mediated cytotoxicity

TL;DR: It is reported that NK cells express Apo-2L and that IL-2 activated CD3(-)NK cells utilize the Apo1L pathway in mediating target cell lysis, indicating an important and distinct role for Apo2L in apoptotic cell destruction.
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Fas ligand expression in the bone marrow in myelodysplastic syndromes correlates with FAB subtype and anemia, and predicts survival.

TL;DR: In MDS, FasL expression in the initial diagnostic BM was higher in patients who were more anemic, correlated directly with red cell transfusion requirements over the subsequent course of the disease, and was predictive of survival, and suggest that pharmacological blockade of the Fas-FasL pathway may be of clinical benefit.
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CD95 ligand: lethal weapon against malignant glioma?

TL;DR: Although several issues regarding glioma cell sensitivity to CD95L/CD95‐mediated apoptosis await elucidation, CD95 is a promising target for the treatment of malignant gliomas.
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Deregulated apoptosis is a hallmark of the Fanconi anemia syndrome.

TL;DR: It is shown that, although demonstrating a high frequency of spontaneous apoptosis, FA cells from four genetic complementation groups are deficient in gamma-ray-induced apoptosis and their MMC hypersensitivity is not due to apoptosis.
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.
Journal ArticleDOI

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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