Immunology of myasthenia gravis.
Anti-acetylcholine-receptor antibody is demonstrable in more than 90 per cent of patients with myasthenia gravis. Serum antibody titers do not show a direct correlation with disease severity, although in certain patients antibody levels increase in association with disease activity. Impairment of neuromuscular transmission results from the loss of junctional receptors, either as a result of receptor internalization or destruction of junctional folds containing the acetylcholine receptor. Myasthenia gravis manifests immunologic, genetic, and clinical similarities to rheumatic syndromes, suggesting a generic immune dysfunction common to these disorders.
D000109:Acetylcholine / Q000378:metabolism; D000911:Antibodies, Monoclonal / Q000276:immunology; D001323:Autoantibodies / Q000276:immunology; D001327:Autoimmune Diseases / Q000276:immunology*; D001667:Binding, Competitive; D002800:Cholinesterase Inhibitors / Q000627:therapeutic use; D003176:Complement C3 / Q000276:immunology; D003186:Complement C9 / Q000276:immunology; D005260:Female; D006801:Humans; D007116:Immunization, Passive; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D008297:Male; D008565:Membrane Proteins / Q000276:immunology; D009157:Myasthenia Gravis / Q000188:drug therapy / Q000276:immunology*; D010956:Plasmapheresis; D011950:Receptors, Cholinergic / Q000276:immunology; D012910:Snake Venoms / Q000378:metabolism; D013570:Synaptic Membranes / Q000648:ultrastructure
D000911:Antibodies, Monoclonal; D001323:Autoantibodies; D002800:Cholinesterase Inhibitors; D003176:Complement C3; D003186:Complement C9; D007166:Immunosuppressive Agents; D008565:Membrane Proteins; D011950:Receptors, Cholinergic; D012910:Snake Venoms; D000109:Acetylcholine