Sieb Joern P
Department of Neurology, Geriatrics and Palliative Care, General Hospital, Grosse Parower St 47-53, Stralsund, 18410 Germany.
Curr Opin Pharmacol. 2005 Jun;5(3):303-7. doi: 10.1016/j.coph.2005.01.010.
Myasthenia gravis is probably the most thoroughly understood of all human autoimmune diseases. The basic mechanism of the disease is an antibody-mediated autoimmune attack that decreases the acetylcholine receptor density at the neuromuscular junction. Current therapies aim to restore the available acetylcholine receptors, deplete the autoantibodies or suppress the immune system. Prolonged drug treatment is required, but this carries a potential risk of severe adverse effects. Therefore, the ideal treatment for myasthenia would eliminate the abnormal autoimmune response without interfering with the immune system.
重症肌无力可能是所有人类自身免疫性疾病中了解最为透彻的一种。该疾病的基本机制是抗体介导的自身免疫攻击,会降低神经肌肉接头处的乙酰胆碱受体密度。目前的治疗方法旨在恢复可用的乙酰胆碱受体、消耗自身抗体或抑制免疫系统。需要长期药物治疗,但这存在严重不良反应的潜在风险。因此,重症肌无力的理想治疗方法是在不干扰免疫系统的情况下消除异常的自身免疫反应。