Graus Y M, De Baets M H
Department of Immunology, University of Limburg, Maastricht, The Netherlands.
Immunol Res. 1993;12(1):78-100. doi: 10.1007/BF02918370.
Myasthenia gravis (MG) is an organ-specific autoimmune disease caused by an antibody-mediated assault on the muscle nicotinic acetylcholine receptor (AChR) at the neuromuscular junction. Binding of antibodies to the AChR leads to loss of functional AChRs and impairs the neuromuscular signal transmission, resulting in muscular weakness. Although a great deal of information on the immunopathological mechanisms involved in AChR destruction exists due to well-characterized animal models, it is not known which etiological factors determine the susceptibility for the disease. This review gives an overview of the literature on the AChR, MG and experimental models for this autoimmune disease.
重症肌无力(MG)是一种器官特异性自身免疫性疾病,由抗体介导对神经肌肉接头处肌肉烟碱型乙酰胆碱受体(AChR)的攻击所致。抗体与AChR结合导致功能性AChR丧失,损害神经肌肉信号传递,从而导致肌肉无力。尽管由于特征明确的动物模型,关于AChR破坏所涉及的免疫病理机制已有大量信息,但尚不清楚哪些病因因素决定了该病的易感性。本文综述了有关AChR、MG以及这种自身免疫性疾病实验模型的文献。