Burres S A, Crayton J W, Gomez C M, Richman D P
Ann Neurol. 1981 Jun;9(6):563-8. doi: 10.1002/ana.410090609.
To investigate individual components of the humoral immune response directed against the acetylcholine receptor in experimental myasthenia, we injected monoclonal antireceptor antibody into normal rats. These antibodies were produced by cloned hybridoma lines formed by fusion of immune spleen cells with the myeloma cell line P3-X63-Ag8. Antibodies from two of seven clones induced acute experimental myasthenia, manifested by clinical weakness, decremental electromyographic response to repetitive nerve stimulation, and diminished mean amplitudes of miniature end-plate potentials (mepps): 0.55 +/- 0.02 mv (SEM) versus 0.71 mv for controls (p less than 0.001). In clinically affected animals, mepp amplitudes from the diaphragm correlated with decremental responses in the gastronemius muscle (r = -0.91, p less than 0.01). The results suggest that binding of a single antibody species to a single determinant on the acetylcholine receptor molecule is sufficient to induce acute experimental myasthenia gravis.
为研究实验性重症肌无力中针对乙酰胆碱受体的体液免疫反应的各个成分，我们将单克隆抗受体抗体注射到正常大鼠体内。这些抗体由免疫脾细胞与骨髓瘤细胞系P3-X63-Ag8融合形成的克隆杂交瘤细胞系产生。七个克隆中有两个克隆产生的抗体诱发了急性实验性重症肌无力，表现为临床肌无力、对重复神经刺激的肌电图反应递减，以及微小终板电位（mepps）平均幅度减小：0.55±0.02毫伏（标准误），而对照组为0.71毫伏（p<0.001）。在出现临床症状的动物中，膈肌的mepp幅度与腓肠肌的递减反应相关（r = -0.91，p<0.01）。结果表明，单一抗体与乙酰胆碱受体分子上的单一决定簇结合足以诱发急性实验性重症肌无力。
