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首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Gene-expression profiling of the early stages of MOG-induced EAE proves EAE-resistance as an active process.
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Gene-expression profiling of the early stages of MOG-induced EAE proves EAE-resistance as an active process.

机译：MOG诱导的EAE早期阶段的基因表达谱证明了EAE抗性是一个活跃的过程。

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摘要

Experimental autoimmune encephalomyelitis (EAE) induced by myelin oligodendrocyte glycoprotein (MOG) is a well-established animal model of multiple sclerosis (MS) in rodents. It reflects the wide spectrum of disease pathology and serves as a valuable tool for studying the pathogenesis and for testing new therapies of MS. In order to identify genes responsible for resistance to and modulation of the disease, we compared the mRNA expression profile of more than 12,000 genes by DNA microarray technique in lymph nodes of the highly EAE-susceptible mouse strain C57Bl/6 (B6) and the resistant strain C57Bl/10.S (B10). The disease onset in B6 mice was day 15. We identified 84 genes that were up-regulated more than two-fold in B10 mice compared to vehicle-treated controls, whereas only two genes were up-regulated in B6 mice after 7 and 15 days post-immunization (p.i.), respectively. We were able to match five up-regulated genes in B10 mice to known quantitative trait loci (QTLs), which control for EAE susceptibility. Only 17, respectively 5, genes were down-regulated at both time points in B10 and B6 mice. Tests for immunoreactivity to MOG (T cell proliferation and interferon-gamma (IFN-gamma) secretion) revealed no stronger immune response in B6 compared to B10 mice supporting the hypothesis of an immunosuppressive effect as a target to prevent EAE in the B10 mice. We conclude that resistance to EAE (and possibly to MS) is an active process mediated by multiple genes up-regulated in peripheral lymphatic organs of resistant animals. Thus, monitoring of the expression of these new candidate genes may serve as a tool for the disease progression and the pharmaceutical treatment.
机译：髓鞘少突胶质细胞糖蛋白（MOG）诱导的实验性自身免疫性脑脊髓炎（EAE）是在啮齿动物中建立的多发性硬化症（MS）动物模型。它反映了广泛的疾病病理学，并且是研究MS的发病机理和测试新疗法的宝贵工具。为了鉴定负责抵抗和调节疾病的基因，我们通过DNA芯片技术比较了在高度EAE易感小鼠品系C57Bl / 6（B6）和耐药株的淋巴结中超过12,000个基因的mRNA表达谱菌株C57B1 / 10.S（B10）。 B6小鼠的疾病发作是在第15天。我们发现与媒介物处理的对照组相比，B10小鼠的84个基因被上调了两倍以上，而B6小鼠在7天和15天后只有两个基因被上调了。免疫后（pi）。我们能够将B10小鼠中的五个上调基因与已知的定量性状基因座（QTL）匹配，该基因控制EAE的易感性。在B10和B6小鼠的两个时间点，只有17个基因，5个基因被下调。对MOG的免疫反应性测试（T细胞增殖和干扰素-γ（IFN-γ）分泌）显示，与B10小鼠相比，B6没有更强的免疫反应，支持了将免疫抑制作用作为预防B10小鼠EAE的靶点的假设。我们得出结论，对EAE（可能还有对MS）的抗性是由抗性动物外周淋巴器官中上调的多个基因介导的一个活跃过程。因此，监测这些新候选基因的表达可作为疾病进展和药物治疗的工具。

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