The lpr and gld genes in systemic autoimmunity: life and death in the Fas lane.
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.
D000818:Animals; D000954:Antigens, Surface / Q000235:genetics / Q000502:physiology*; D017209:Apoptosis / Q000235:genetics*; D001327:Autoimmune Diseases / Q000235:genetics*; D015551:Autoimmunity / Q000235:genetics*; D001402:B-Lymphocytes / Q000276:immunology / Q000473:pathology; D004195:Disease Models, Animal; D005796:Genes; D007108:Immune Tolerance / Q000235:genetics; D008024:Ligands; D008180:Lupus Erythematosus, Systemic / Q000235:genetics*; D008232:Lymphoproliferative Disorders / Q000235:genetics*; D008565:Membrane Proteins / Q000235:genetics / Q000502:physiology*; D051379:Mice; D008817:Mice, Mutant Strains / Q000235:genetics / Q000276:immunology*; D010641:Phenotype; D011828:Radiation Chimera; D016176:T-Lymphocyte Subsets / Q000276:immunology / Q000473:pathology; D013950:Thymus Gland / Q000473:pathology; D019014:fas Receptor
D000954:Antigens, Surface; D008024:Ligands; D008565:Membrane Proteins; D019014:fas Receptor