Molina-Holgado E, Areválo-Martín A, Vela J M, Guaza C
Instituto Cajal. CSIC, Madrid, España.
Rev Neurol. 2002;35(10):973-8.
Theiler's murine encephalomyelitis virus (TMEV) disease is induced following intracerebral inoculation of TMEV, a member of picornavirus family, in susceptible animals. The pathogenesis of paralytic syndrome is associated with a chronic progressive demyelinating disease characterized by perivascular of immune inflammatory cells. Although TMEV induced demyelinating disease (TMEV IDD) is initiated by virus specific CD4+ T cells targeting CNS persistent virus, CD4+ T cell responses against self myelin epitopes activated via epitope spreading contribute to chronic disease pathogenesis. In the present report we delineated possible pathogenic mechanisms related with inflammatory process, leading to demyelination and axonal loss. The importance of proinflammatory cytokines in sustaining the inflammatory process and cause direct oligodendrotoxicity is emphasized. Different approaches in therapeutic strategies affecting cytokines are also presented.
将脑心肌炎病毒（TMEV）接种到易感动物脑内后，可诱发Theiler小鼠脑脊髓炎病毒（TMEV）疾病。TMEV属于微小核糖核酸病毒科，麻痹综合征的发病机制与一种以血管周围免疫炎症细胞为特征的慢性进行性脱髓鞘疾病有关。虽然TMEV诱导的脱髓鞘疾病（TMEV IDD）是由靶向中枢神经系统持续性病毒的病毒特异性CD4 + T细胞引发的，但通过表位扩展激活的针对自身髓鞘表位的CD4 + T细胞反应有助于慢性疾病的发病机制。在本报告中，我们阐述了与炎症过程相关的可能致病机制，该机制导致脱髓鞘和轴突损失。强调了促炎细胞因子在维持炎症过程和引起直接少突胶质细胞毒性方面的重要性。还介绍了影响细胞因子的治疗策略中的不同方法。
