Barnett L A, Whitton J L, Wang L Y, Fujinami R S
Department of Neurology, University of Utah, Salt Lake City 84132, USA.
J Neuroimmunol. 1996 Feb;64(2):163-73. doi: 10.1016/0165-5728(95)00165-4.
The association of viral infections with autoimmune central nervous system (CNS) diseases such as post-infectious encephalomyelitis and possibly multiple sclerosis (MS) prompted the investigation to understand how virus infection could modulate autoimmune responses. Recombinant vaccinia viruses encoding an encephalitogenic portion of myelin basic protein (MBP) were evaluated in an animal model for human demyelinating disease, experimental allergic encephalomyelitis (EAE). We have determined that mice vaccinated with recombinant viruses encoding an encephalitogenic region of MBP were protected from EAE. In vivo depletion of CD8+ T cells did not abrogate this protection, suggesting lack of regulation by this cell type. These studies demonstrate that virus infection may be a means to modulated immune responsiveness to CNS disease.
病毒感染与自身免疫性中枢神经系统(CNS)疾病(如感染后脑脊髓炎以及可能的多发性硬化症(MS))之间的关联促使人们展开研究,以了解病毒感染如何调节自身免疫反应。在一种人类脱髓鞘疾病——实验性变应性脑脊髓炎(EAE)的动物模型中,对编码髓鞘碱性蛋白(MBP)致脑炎部分的重组痘苗病毒进行了评估。我们已经确定,接种了编码MBP致脑炎区域的重组病毒的小鼠对EAE具有抵抗力。体内CD8 + T细胞的耗竭并未消除这种保护作用,这表明该细胞类型缺乏调节作用。这些研究表明,病毒感染可能是调节对CNS疾病免疫反应性的一种手段。