Williams R M, Krakowka S, Koestner A
Acta Neuropathol. 1980;50(1):1-8. doi: 10.1007/BF00688528.
Central nervous system (CNS) myelin-specific antiserum was capable of initiating primary demyelination within 24 h following injection into the dorsal column of guinea pig spinal cord. Control serum injected in the same manner did not produce demyelination. The demyelinating lesions occurred as focal linear plaques of completely denuded intact axons surrounded by partially demyelinated and myelinated normal axons. Antiserum-mediated demyelination was followed by mononuclear cell infiltration 7-10 days later. Ultrastructural examination revealed vesiculation of myelin followed by cleavage of myelin lamellae at the intraperiod line. Remyelination began between 7 and 10 days following injection and correlated well with clinical evidence of recovery. The results of this study point to the importance of circulating antimyelin antibodies in the pathogenesis of demyelinating encephalitis. The model represents an in vivo approach to the study of the pathogenesis of immune-mediated myelinolysis in demyelinating disorders like multiple sclerosis (MS), subacute sclerosing panencephalitis (SSPE), and canine distemper encephalitis (CDE).
中枢神经系统(CNS)髓鞘特异性抗血清在注入豚鼠脊髓背柱后24小时内能够引发原发性脱髓鞘。以相同方式注射的对照血清未产生脱髓鞘。脱髓鞘病变表现为局灶性线性斑块,由完全裸露的完整轴突组成,周围是部分脱髓鞘和有髓鞘的正常轴突。抗血清介导的脱髓鞘7 - 10天后出现单核细胞浸润。超微结构检查显示髓鞘形成水泡,随后在周期间线处髓鞘板层裂开。注射后7至10天开始重新髓鞘化,且与恢复的临床证据密切相关。本研究结果表明循环抗髓鞘抗体在脱髓鞘性脑炎发病机制中的重要性。该模型代表了一种体内研究方法,用于研究像多发性硬化症(MS)、亚急性硬化性全脑炎(SSPE)和犬瘟热脑炎(CDE)等脱髓鞘疾病中免疫介导的髓鞘溶解的发病机制。