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首页> 外文期刊>Serbian Journal of Experimental and Clinical Research >Latent Murine Cytomegalovirus Infection Contributes to EAE Pathogenesis / Latentna Infekcija Mi?jim Citomegalovirusom Ima Ulogu U Patogenezi Eksperimentalnog Autoimunskog Encefalomijelitisa
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Latent Murine Cytomegalovirus Infection Contributes to EAE Pathogenesis / Latentna Infekcija Mi?jim Citomegalovirusom Ima Ulogu U Patogenezi Eksperimentalnog Autoimunskog Encefalomijelitisa

机译：潜在的小鼠巨细胞病毒潜伏性感染导致EAE发病机理/小鼠巨细胞病毒的潜伏感染在实验性自身免疫性脑脊髓炎的发病机理中具有重要作用

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ABSTRACT Viral infection has been identified as the most likely environmental trigger of multiple sclerosis (MS). There are conflicting data regarding the role of cytomegalovirus (CMV) in MS pathogenesis. We utilised experimental autoimmune encephalomyelitis (EAE)-resistant BALB/c mice and murine cytomegalovirus (MCMV), the murine homolog of CMV, to examine the mechanism by which viral infection enhances autoimmune neuroinflammation. Mice subjected to latent neonatal MCMV infection developed the typical characteristics of EAE. Similar to MS, the MCMV-infected EAE-induced mice developed infiltrates in the central nervous system (CNS) composed of similar percentages of CD4+ and CD8+ T cells. The influx of both Th 1 and Th 17 cells into the CNS of MCMV- infected EAE-induced mice was observed. Interestingly, the development of autoimmune neuroinflammation after latent MCMV infection was accompanied by a significant influx of Tc17 cells (CD8+IL-17+ and CD8+RoRγt+) but not Tc1, cells. Our results suggest that latent MCMV infection affects the development of inflammatory lymphocytes that exhibit encephalitogenic potential, thereby mediating increased CNS pathology following EAE induction, and that CMV represents a possible environmental factor in the pathogenesis of MS and other autoimmune diseases.
机译：摘要病毒感染已被确定为多发性硬化症（MS）最可能的环境触发因素。关于巨细胞病毒（CMV）在MS发病机制中的作用，存在相互矛盾的数据。我们利用实验性自身免疫性脑脊髓炎（EAE）耐药的BALB / c小鼠和鼠巨细胞病毒（MCMV）（CMV的鼠类同源物）来研究病毒感染增强自身免疫性神经炎症的机制。新生儿MCMV潜伏感染的小鼠表现出EAE的典型特征。与MS相似，MCMV感染的EAE诱导的小鼠在中枢神经系统（CNS）中形成浸润，由相同百分比的CD4 +和CD8 + T细胞组成。观察到Th 1和Th 17细胞均流入MCMV感染的EAE诱导的小鼠的中枢神经系统。有趣的是，MCMV潜伏感染后自身免疫性神经炎症的发展伴随着Tc17细胞（CD8 + IL-17 +和CD8 +RoRγt+）的大量涌入，而Tc1细胞却没有。我们的结果表明，潜在的MCMV感染会影响具有脑致病潜力的炎性淋巴细胞的发育，从而介导EAE诱导后CNS病理的增加，而CMV代表了MS和其他自身免疫性疾病发病机理中的可能环境因素。

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