Acetylcholine receptor antibodies in the diagnosis of human and experimental myasthenia gravis

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Abstract
Aspects of acetylcholine receptor immunology and circulating receptor antibodies are reviewed with regard to both human and experimental myasthenia gravis. Receptor antibodies that have negligible cross‐reactivity with skeletal muscle receptor can nonetheless cause destruction of the postsynaptic motor endplate area. Antibodies to mammalian skeletal muscle receptor can bind in‐situ receptors. Transfer of myasthenic IgG increases neurophysiologic symptoms in rabbits showing slight sings of experimental myasthenia gravis, suggesting a block of in‐situ receptors. Determination of receptor antibodies using RIA tests and partially purified human skeletal muscle receptor has been evaluated in the diagnosis of myasthenia gravis. Ninety percent of Swedish myasthenic patients in one study were found to have receptor antibodies. A rough correlation has been found between antibody titer and the severity of disease. Immunosuppressive treatment and thymectomy decrease the titer. In patients with thymoma, high antibody titers remain. When taken together, antibody‐titer determination and electrophysiologic tests–particularly single‐fiber electromyography–are very valuable diagnostic tools.