Buschman E, van Oers N, Katz M, Murgita R A
J Neuroimmunol. 1987 Jan;13(3):315-30. doi: 10.1016/0165-5728(87)90067-1.
The induction of experimental autoimmune myasthenia gravis (EAMG) was studied by the passive transfer of gamma-globulin from myasthenia gravis (MG) patients to C57BL/6 mice. Muscular weakness and electromyographic decrements (EMG) could be consistently induced in all mice injected with gamma-globulin from certain selected MG patients. There was, however, no correlation between the antiacetylcholine receptor antibody titre in the donor gamma-globulin and the ability to induce EAMG. The possible beneficial effects of immunoregulatory alpha-fetoprotein (AFP) treatment were investigated employing the passive EAMG model. Mice were protected against the onset of severe symptoms provided the AFP was administered before and after passive transfer. The exaggerated fatigue characteristics associated with murine EAMG as detected by EMG could be alleviated by AFP treatment. These findings raise the possibility that AFP may be of some therapeutic value in the control of MG.
通过将重症肌无力（MG）患者的γ球蛋白被动转移至C57BL/6小鼠来研究实验性自身免疫性重症肌无力（EAMG）的诱导情况。在所有注射了某些特定MG患者γ球蛋白的小鼠中，均可持续诱发肌无力和肌电图衰减（EMG）。然而，供体γ球蛋白中的抗乙酰胆碱受体抗体滴度与诱导EAMG的能力之间并无相关性。利用被动EAMG模型研究了免疫调节性甲胎蛋白（AFP）治疗的可能有益效果。如果在被动转移前后给予AFP，则可保护小鼠免于出现严重症状。通过AFP治疗可缓解由EMG检测到的与鼠EAMG相关的过度疲劳特征。这些发现增加了AFP在控制MG方面可能具有一定治疗价值的可能性。
