Abstract
Autoantibodies directed at the extracellular domain of skeletal muscle nicotinic acetylcholine receptors (AChRs), especially those directed at the main immunogenic region (MIR) at the extracellular tip of α1 subunits, mediate the immune assault that impairs neuromuscular transmission, thereby causing the weakness and fatigability characteristic of myasthenia gravis (MG).1 Immunizing animals with AChRs purified from fish electric organs, or mammalian muscle, or with chimeras of human α1 subunits in AChR-related mollusk acetylcholine binding proteins, or with the mollusk protein itself, initiates an animal model of MG.2 What triggers formation of autoantibodies to AChRs in MG is not known. It is frequently speculated …
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