Simpson J A, Behan P O, Dick H M
Ann N Y Acad Sci. 1976;274:382-9. doi: 10.1111/j.1749-6632.1976.tb47699.x.
Clinical and laboratory data continue to support the concept of a genetically determined breakdown of immunological tolerance in myasthenia gravis with immunological damage to the motor end plates. The demonstration of impaired function of thymus-derived lymphocytes and of IgA deficiency correlate well with the clinical data in which there is an increase incidence of autoimmune diseases associated with anergy. Whilst the exact pathogenesis of myasthenia gravis is unknown, the available data support the concept of an immune deficiency disorder.
重症肌无力存在基因决定的免疫耐受破坏，伴有运动终板的免疫损伤。胸腺来源淋巴细胞功能受损及IgA缺乏的证明与临床数据密切相关，临床数据显示自身免疫性疾病发生率增加且伴有无反应性。虽然重症肌无力的确切发病机制尚不清楚，但现有数据支持免疫缺陷疾病的概念。
