Vincent A, Newsom Davis J
J Neurol Neurosurg Psychiatry. 1980 Jul;43(7):590-600. doi: 10.1136/jnnp.43.7.590.
Early suggestions that a humoral factor might be implicated in the disorder of neuromuscular transmission in myasthenia gravis have been confirmed by the detection of anti-AChR antibody in 85-90% of the patients with generalised disease and in 75% of cases with restricted ocular myasthenia. Plasma exchange reveals that serum anti-AChR usually has an inverse relationship to muscle strength and present evidence indicates that patients responding to thymectomy and immunosuppressive drug treatment usually show a consistent decline in serum anti-AChR titres. The antibody is heterogeneous and can lead to a loss of muscle AChR by several mechanisms. Anti-AChR is produced in the thymus in relatively small amounts. Anti-AChR antibody synthesis by thymic lymphocytes and pokeweed stimulated peripheral lymphocytes in culture provides a means of studying the effect of different lymphocyte populations in vitro. Analysis of clinical, immunological and HLA antigen characteristics in MG suggest that more than one mechanism may underlie the breakdown in tolerance to AChR, leading to the production of anti-AChR antibodies.
早期关于体液因素可能与重症肌无力神经肌肉传递障碍有关的推测，已被以下发现所证实：在85% - 90%的全身型患者以及75%的局限性眼肌型患者中检测到了抗乙酰胆碱受体（AChR）抗体。血浆置换显示，血清抗AChR通常与肌肉力量呈负相关，现有证据表明，对胸腺切除术和免疫抑制药物治疗有反应的患者，其血清抗AChR滴度通常会持续下降。该抗体具有异质性，可通过多种机制导致肌肉AChR丧失。抗AChR在胸腺中少量产生。胸腺淋巴细胞和商陆刺激的外周淋巴细胞在体外培养时合成抗AChR抗体，为研究不同淋巴细胞群体在体外的作用提供了一种方法。对重症肌无力患者的临床、免疫学和HLA抗原特征分析表明，可能有不止一种机制导致对AChR的耐受性破坏，从而产生抗AChR抗体。
