Childs L A, Harrison R, Lunt G G
J Neuroimmunol. 1985 Jul;9(1-2):69-80. doi: 10.1016/s0165-5728(85)80007-2.
The toxicity of myasthenic sera to rat myotubes in monolayer culture was examined by measuring the release of [Me-3H]carnitine from pre-loaded cells. In the presence of guinea pig complement, heat-inactivated serum samples from 9 out of 13 myasthenic patients showed clear myotoxicity, in contrast to 0 out of 11 normal controls and 0 out of 6 polymyositis patients. Neither heat-inactivated sera alone nor guinea pig complement sera alone showed myotoxicity. Removal of anti-acetylcholine receptor (anti-AChR) antibodies from a myasthenic serum sample by affinity absorption led to loss of myotoxicity. Myotoxicity of myasthenic sera could, in most cases, be confirmed by light microscopy. These results support the idea that complement-mediated cell damage, initiated by anti-AChR antibodies, contributes to post-synaptic membrane degeneration in myasthenia gravis.
通过测量预先加载的细胞中[甲基 - 3H]肉碱的释放,研究了重症肌无力血清对单层培养的大鼠肌管的毒性。在豚鼠补体存在的情况下,13例重症肌无力患者中有9例的热灭活血清样本表现出明显的肌毒性,相比之下,11例正常对照者中无1例出现肌毒性,6例多发性肌炎患者中也无1例出现肌毒性。单独的热灭活血清或单独的豚鼠补体血清均未表现出肌毒性。通过亲和吸附从重症肌无力血清样本中去除抗乙酰胆碱受体(抗AChR)抗体后,肌毒性消失。在大多数情况下,重症肌无力血清的肌毒性可通过光学显微镜确认。这些结果支持了这样一种观点,即由抗AChR抗体引发的补体介导的细胞损伤,促成了重症肌无力中突触后膜的退化。