Pachner A R
Department of Neurology, Georgetown University School of Medicine, Washington, DC 20007.
Neurology. 1989 Aug;39(8):1057-61. doi: 10.1212/wnl.39.8.1057.
We assayed sera from 20 myasthenics of various clinical stages and anti-acetylcholine receptor (AChR) antibody levels for their ability to affect bungarotoxin (BGT) binding to native human AChR on the surface of TE671 cells. Thirty-five percent of sera blocked BGT binding to the AChR, some at a dilution of up to 1:1000. The 7 patients whose sera blocked toxin binding were all generalized myasthenics with particularly severe disease, 6 of whom had had myasthenic crisis at some point in their course. No ocular myasthenics had blocking antibody. Blockade of toxin binding by myasthenic antibody to TE671 cells resembled blockade produced by unlabeled toxin in being irreversible with washing. There was little correlation between ability to block toxin binding and amplitude of the AChR binding antibody. These data are consistent with the hypothesis that patients with more aggressive generalized myasthenia preferentially have anti-AChR antibody that blocks toxin binding.
我们检测了20名处于不同临床阶段的重症肌无力患者的血清及其抗乙酰胆碱受体（AChR）抗体水平，以评估其影响银环蛇毒素（BGT）与TE671细胞表面天然人AChR结合的能力。35%的血清可阻断BGT与AChR的结合，有些血清在高达1:1000的稀释度下仍有阻断作用。血清能阻断毒素结合的7名患者均为全身型重症肌无力患者，病情尤其严重，其中6人在病程中的某个阶段曾发生过重症肌无力危象。眼肌型重症肌无力患者均无阻断抗体。重症肌无力抗体对TE671细胞毒素结合的阻断作用与未标记毒素产生的阻断作用相似，洗涤后不可逆转。毒素结合阻断能力与AChR结合抗体的幅度之间几乎没有相关性。这些数据与以下假设一致，即病情更严重的全身型重症肌无力患者优先产生能阻断毒素结合的抗AChR抗体。
