Monoclonal antibody to Theiler's murine encephalomyelitis virus defines a determinant on myelin and oligodendrocytes, and augments demyelination in experimental allergic encephalomyelitis.
Monoclonal antibody to Theiler's murine encephalomyelitis virus defines a determinant on myelin and oligodendrocytes, and augments demyelination in experimental allergic encephalomyelitis.
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泰勒氏鼠脑脊髓炎病毒的单克隆抗体定义了髓鞘质和少突胶质细胞的决定因素，并增强了实验性过敏性脑脊髓炎的脱髓鞘作用。
DOI：
10.1084/jem.171.6.1893
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Fujinami,RS
中科院分区：
文献类型：
--
作者：
Yamada,M;Zurbriggen,A;Fujinami,RS
多年来，已知泰勒病毒可引起小鼠脑脊髓炎（1，2），并被归类为小核糖核酸病毒家族（3）。Theiler鼠脑脊髓炎病毒（TMEV）的DA毒株可在小鼠中引起双相中枢神经系统（CNS）疾病（4）：急性脊髓灰质炎脑脊髓炎和/或慢性炎性脱髓鞘疾病，这取决于病毒的剂量和毒株以及小鼠的遗传背景。TMEV诱导的CNS疾病是人类脱髓鞘疾病的动物模型，包括感染后脑脊髓炎和多发性硬化（4-6）。已经提出影响少突胶质细胞和/或髓磷脂的直接病毒（7-10）和免疫介导的（11-13）机制均引发CNS内的炎症事件，导致慢性脱髓鞘。免疫介导的机制包括：“无辜旁观者”理论;病毒感染对少突胶质细胞的免疫损伤;以及病毒诱导的自身免疫事件（5，6，14，15）。自身免疫事件可以通过对由少突胶质细胞的病毒感染继发释放的髓鞘抗原的致敏来诱导，或者通过病毒和髓鞘组分之间存在共同表位来诱导，从而导致交叉反应性免疫应答。我们已经提出了一种机制，其中病毒可以通过拥有与自身组分共同或交叉反应的决定簇（分子模拟）来引发或增强自身免疫性疾病（16）。在早期的研究中，我们发现针对病毒前体的单克隆抗体，
Theiler's viruses have been known for many years to cause an encephalomyelitis in mice (1, 2), and have been classified in the picornavirus family (3). The DA strain of Theiler's murine encephalomyelitis viruses (TMEV)'can cause a biphasic central nervous system (CNS) disease in mice (4): acute polioencephalomyelitis and/or chronic inflammatory demyelinating disease, depending on the dose and strain of the virus and genetic background of the mouse. The former is clearly the result of direct viral cytopathic effects, while the pathogenesis of the latter is under intense exploration.The CNS disease induced by TMEV is an animal model for human demyelinating diseases, including post-infectious encephalomyelitis and multiple sclerosis (4-6). Both direct viral (7-10) and immune-mediated (11-13) mechanisms affecting oligodendrocytes and/or myelin have been proposed to initiate inflammatory events within the CNS, leading to the chronic demyelination. Immune-mediated mechanisms include an:" innocent bystander" theory; immunologic injury to oligodendrocytes infected with virus; and virus-induced autoimmune events (5, 6, 14, 15). Autoimmune events may be induced by sensitization to myelin antigens that are secondarily released by viral infection of oligodendrocytes, or induced by the presence of a common epitope between virus and myelin components resulting in crossreactive immune response. We have proposed a mechanism in which viruses may initiate or enhance autoimmune diseases by possessing common or crossreacting determinants (molecular mimicry) with self components (16). In earlier studies, we found that mAbs to viral pro-