Rodriguez M, Oleszak E, Leibowitz J
Mayo Medical School, Rochester, Minnesota.
Crit Rev Immunol. 1987;7(4):325-65.
Theiler's murine encephalomyelitis virus (TMEV) causes immune-mediated demyelination in susceptible mice which is similar to human demyelinating disorders such as multiple sclerosis. In addition, the picornavirus persists within the central nervous system throughout the course of the chronic demyelinating disease. This article reviews the neuropathology, virology, immunology, and molecular biology of the model system. We analyze the possible mechanisms by which this virus induces demyelination and persists in the nervous system. Finally, we provide a hypothesis that the specificity of primary white matter destruction in the TMEV model depends on immune-sensitized cells which interact with viral antigen plus major histocompatibility complex (MHC) antigens on the surfaces of oligodendrocytes or myelin sheaths.
泰勒氏鼠脑脊髓炎病毒（TMEV）可在易感小鼠中引发免疫介导的脱髓鞘，这与人类脱髓鞘疾病如多发性硬化症相似。此外，这种小核糖核酸病毒在慢性脱髓鞘疾病的整个病程中都持续存在于中枢神经系统内。本文综述了该模型系统的神经病理学、病毒学、免疫学和分子生物学。我们分析了这种病毒诱导脱髓鞘并在神经系统中持续存在的可能机制。最后，我们提出一个假说，即TMEV模型中原发性白质破坏的特异性取决于与少突胶质细胞或髓鞘表面的病毒抗原加主要组织相容性复合体（MHC）抗原相互作用的免疫致敏细胞。
