Abstract
Fas ligand (FasL) is a death factor that binds to its receptor, Fas, and induces apoptosis. Two mutations that accelerate autoimmune disease, lpr and gld, are known to correspond to mutations within genes encoding Fas and FasL, respectively. Here, Shigekazu Nagata and Takashi Suda summarize current knowledge of Fas and FasL, and discuss the physiological role of the Fas system in T-cell development, cytotoxicity and cytotoxic T lymphocyte (CTL)-mediated autoimmune disease.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Amino Acid Sequence
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Animals
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Antigens, Surface / physiology*
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Apoptosis / physiology
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Autoimmune Diseases / genetics
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Autoimmune Diseases / immunology
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Base Sequence
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Ligands
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Lymphoproliferative Disorders / genetics
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Lymphoproliferative Disorders / immunology
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Mice
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Mice, Mutant Strains
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Molecular Sequence Data
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Mutation*
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Receptors, Cell Surface / immunology
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T-Lymphocytes / immunology
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T-Lymphocytes, Cytotoxic / immunology
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fas Receptor
Substances
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Antigens, Surface
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Ligands
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Receptors, Cell Surface
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fas Receptor