Morphologic and immunologic studies in experimental autoimmune myasthenia gravis and myasthenia gravis.
An indirect immunoperoxidase technique was used to study by light microscopy the binding of serum from experimental autoimmune myasthenia gravis (EAMG) rabbits to junctionally and extrajunctionally located acetylcholine receptors (AChRs) in human and rat muscles. Binding was restricted to junctional AChR. Alpha bungarotoxin (a-BGT) partially blocked the binding of EAMG serum, while myasthenia gravis serum, carbamylcholine, decamethonium, and tubocurarine did not. A radioimmunoassay showed significant binding of antibodies in EAMG sera to 125l AChR. This binding was not inhibited by a-BGT, nor by carbamylcholine, decamethonium, or tubocurarine. Sera from 10 myasthenia gravis patients did not contain antibodies binding to the 125l AChR. We suggest that EAMG in rabbits induced by Torpedo AChR differs serologically from myasthenia gravis in patients, probably owing to antigenic differences between Torpedo and human AChR, and that antigenic differences also exist between junctional and extrajunctional receptors.
D000109:Acetylcholine / Q000378:metabolism; D000818:Animals; D000917:Antibody Formation; D001327:Autoimmune Diseases / Q000276:immunology*; D001666:Binding Sites, Antibody; D002038:Bungarotoxins / Q000494:pharmacology; D002217:Carbachol / Q000494:pharmacology; D003650:Decamethonium Compounds / Q000494:pharmacology; D004195:Disease Models, Animal; D000939:Epitopes; D006801:Humans; D009157:Myasthenia Gravis / Q000276:immunology*; D011817:Rabbits; D011863:Radioimmunoassay; D011950:Receptors, Cholinergic / Q000276:immunology / Q000378:metabolism; D014403:Tubocurarine / Q000494:pharmacology
D002038:Bungarotoxins; D003650:Decamethonium Compounds; D000939:Epitopes; D011950:Receptors, Cholinergic; D002217:Carbachol; D000109:Acetylcholine; D014403:Tubocurarine