Acetylcholine receptor turnover in myasthenia gravis.
Humoral antibodies directed against the acetylcholine receptor are present in most patients with myasthenia gravis. These antibodies accelerate receptor degradation and thus cause a decrease in receptor level and impaired neuromuscular transmission. The stimulus that triggers and sustains the formation of the antibodies has not been identified, but it is possible that the primary antigen may be located on the cell surface of thymic lymphocytes. In some situations the clinical state in myasthenia gravis does not correlate with the antibody titer, suggesting that other factors also influence receptor amount and/or function of other potential regulators that have been investigated. Calcium and agents that increase cyclic AMP appear to increase the formation of the receptor and thus might serve to mitigate the effects of the circulating antibodies. In contrast, cholinergic agonists may cause a further decrease in receptor number, providing an explanation of why myasthenic patients may become resistant to therapy.
D000818:Animals; D002478:Cells, Cultured; D006801:Humans; D007111:Immunity, Cellular; D007074:Immunoglobulin G; D009132:Muscles / Q000502:physiology; D009157:Myasthenia Gravis / Q000276:immunology / Q000378:metabolism* / Q000628:therapy; D009712:Nucleotides, Cyclic / Q000494:pharmacology; D051381:Rats; D011950:Receptors, Cholinergic / Q000187:drug effects / Q000276:immunology / Q000378:metabolism*; D013934:Thymectomy; D013950:Thymus Gland / Q000276:immunology
D007074:Immunoglobulin G; D009712:Nucleotides, Cyclic; D011950:Receptors, Cholinergic