Abstract
The single gene lpr and gld models of spontaneous systemic autoimmunity have attracted much attention in recent years. Here, Philip Cohen and Robert Eisenberg describe the fascinating recent findings that the lpr and gld [corrected] phenotypes result from defects in the Fas gene and, perhaps, in the ligand for fas, respectively.
MeSH terms
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Animals
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Antigens, Surface / genetics
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Antigens, Surface / physiology*
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Apoptosis / genetics*
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Autoimmune Diseases / genetics*
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Autoimmunity / genetics*
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B-Lymphocytes / immunology
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B-Lymphocytes / pathology
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Disease Models, Animal*
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Genes*
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Immune Tolerance / genetics
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Ligands
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Lupus Erythematosus, Systemic / genetics*
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Lymphoproliferative Disorders / genetics*
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Membrane Proteins / genetics
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Membrane Proteins / physiology*
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Mice
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Mice, Mutant Strains / genetics
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Mice, Mutant Strains / immunology*
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Phenotype
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Radiation Chimera
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T-Lymphocyte Subsets / immunology
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T-Lymphocyte Subsets / pathology
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Thymus Gland / pathology
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fas Receptor
Substances
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Antigens, Surface
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Ligands
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Membrane Proteins
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fas Receptor