Tindall R S, Cloud R, Luby J, Rosenberg R N
Neurology. 1978 Mar;28(3):273-7. doi: 10.1212/wnl.28.3.273.
The etiology of the immunologic abnormalities in myasthenia gravis (MG) remains unknown. Evidence for persistent viral infection was sought by determining serum antibody titers to several enveloped RNA and DNA viruses. Compared to healthy controls matched for age, sex, geography and socioeconomic status, patients with MG were more likely to have elevated titers of complement-fixing antibody to cytomegalovirus (CMV). Patients with MG not treated with thymectomy or steroids had elevated CMV titers, whereas thymectomized or steroid-treated patients did not; the differences were statistically significant (p less than 0.01). These results are consistent with the hypothesis that there is persistent viral antigenic stimulation in the myasthenic thymus, arising from viral protein incorporation into epithelioid-myoid cell surface membranes and subsequent induction of an antibody to these acetylcholine receptor (AChR)-bearing thymic cells. This antibody then cross-reacts with AChR at the neuromuscular junction.
重症肌无力(MG)免疫异常的病因尚不清楚。通过测定针对几种包膜RNA和DNA病毒的血清抗体滴度来寻找持续性病毒感染的证据。与年龄、性别、地理位置和社会经济地位相匹配的健康对照相比,MG患者更有可能对巨细胞病毒(CMV)的补体结合抗体滴度升高。未接受胸腺切除术或类固醇治疗的MG患者CMV滴度升高,而接受胸腺切除术或类固醇治疗的患者则没有;差异具有统计学意义(p小于0.01)。这些结果与以下假设一致,即重症肌无力患者的胸腺中存在持续性病毒抗原刺激,这是由于病毒蛋白掺入上皮样-肌样细胞表面膜,并随后诱导针对这些带有乙酰胆碱受体(AChR)的胸腺细胞产生抗体所致。然后,这种抗体在神经肌肉接头处与AChR发生交叉反应。