Myasthenia gravis: past, present, and future.
Myasthenia gravis (MG) is an autoimmune syndrome caused by the failure of neuromuscular transmission, which results from the binding of autoantibodies to proteins involved in signaling at the neuromuscular junction (NMJ). These proteins include the nicotinic AChR or, less frequently, a muscle-specific tyrosine kinase (MuSK) involved in AChR clustering. Much is known about the mechanisms that maintain self tolerance and modulate anti-AChR Ab synthesis, AChR clustering, and AChR function as well as those that cause neuromuscular transmission failure upon Ab binding. This insight has led to the development of improved diagnostic methods and to the design of specific immunosuppressive or immunomodulatory treatments.
Conti-Fine
Bianca M
BM
Department of Biochemistry, University of Minnesota, Minneapolis, Minnesota 55455, USA. conti001@umn.edu
Milani
Monica
M
Kaminski
Henry J
HJ
D000818:Animals; D049670:History, 17th Century; D049672:History, 19th Century; D049673:History, 20th Century; D049674:History, 21st Century; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D008214:Lymphocytes / Q000276:immunology / Q000378:metabolism; D009157:Myasthenia Gravis / Q000175:diagnosis / Q000188:drug therapy* / Q000266:history / Q000276:immunology*; D009469:Neuromuscular Junction / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D011950:Receptors, Cholinergic / Q000276:immunology / Q000378:metabolism
D007166:Immunosuppressive Agents; D011950:Receptors, Cholinergic