Borrow P, Welsh C J, Tonks P, Dean D, Blakemore W F, Nash A A
Edward Jenner Institute for Vaccine Research, Newbury, Berkshire, UK.
Immunology. 1998 Apr;93(4):478-84. doi: 10.1046/j.1365-2567.1998.00459.x.
The contribution of autoimmune responses to the pathogenesis of Theiler's virus-induced demyelinating disease was investigated. Delayed-type hypersensitivity responses to myelin were examined in both symptomatic and asymptomatic mice at different times post-infection, in order to determine whether autoreactivity correlates with the development of demyelination. The results indicate that although autoimmune responses probably do not play a major role in the initiation of demyelination at early times post-infection, autoreactivity to myelin antigens dose eventually develop in symptomatic animals, perhaps through the mechanism of epitope spreading. Autoimmunity to myelin components is therefore an additional factor that may contribute to lesion progression in chronically diseased animals.
研究了自身免疫反应在泰勒氏病毒诱导的脱髓鞘疾病发病机制中的作用。在感染后的不同时间，对有症状和无症状小鼠的髓鞘迟发型超敏反应进行了检测，以确定自身反应性是否与脱髓鞘的发展相关。结果表明，尽管自身免疫反应在感染后早期脱髓鞘的起始阶段可能不发挥主要作用，但有症状动物最终会出现对髓鞘抗原的自身反应性，这可能是通过表位扩展机制实现的。因此，针对髓鞘成分的自身免疫是可能导致慢性患病动物病变进展的另一个因素。
