现今认为重症肌无力(MG)是随意肌的突触后膜乙酰胆碱受体(AchR)的自身免疫性肌病。即由于血中的抗AchR抗体对受体的封闭使它不能与乙酰胆碱(Ach)有效地结合,抗体受体复合物在补体C_3的参与下可溶解受体;杀伤T细胞及淋巴因子可破坏受体;辅助T细胞可促进B细胞合成抗AchR抗体,这种抗体的大部分在胸腺内合成,T淋巴细胞在胸腺内致敏,引起MG的自身免疫反应的始动抗原也存在于胸腺(即肌样细胞)。因此现今治疗的目标基本是针对抗 Myotonic myasthenia (MG) is nowadays thought to be an autoimmune myopathic disorder of the postsynaptic acetylcholine receptor (AchR) in the voluntary muscle. That is, the blocking of the receptor by the anti-AchR antibody in the blood can not effectively bind with acetylcholine (Ach), and the antibody receptor complex can dissolve the receptor with the participation of complement C_3; the destruction of T-cells and lymphokines can be affected by Body; helper T cells can promote the synthesis of anti-AchR antibodies B cells, most of this antibody synthesis in the thymus, T lymphocytes in the thymus sensitization, causing MG autoimmune reaction of the primed antigen also exists in the thymus (ie Myoid cells). Therefore, the current treatment target is basically against