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首页> 外文期刊>Developmental Immunology: Journal of Immunology Research >Understanding Autoimmune Mechanisms in Multiple Sclerosis Using Gene Expression Microarrays: Treatment Effect and Cytokine-related Pathways
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Understanding Autoimmune Mechanisms in Multiple Sclerosis Using Gene Expression Microarrays: Treatment Effect and Cytokine-related Pathways

机译：使用基因表达芯片了解多发性硬化症的自身免疫机制：治疗效果和细胞因子相关的途径。

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Multiple sclerosis (MS) is a central nervous system disease in which activated autoreactive T-cells invade the blood brain barrier and initiate an inflammatory response that leads to myelin destruction and axonal loss. The etiology of MS, as well as the mechanisms associated with its unexpected onset, the unpredictable clinical course spanning decades, and the different rates of progression leading to disability over time, remains an enigma. We have applied gene expression microarrays technology in peripheral blood mononuclear cells (PBMC) to better understand MS pathogenesis and better target treatment approaches. A signature of 535 genes were found to distinguish immunomodulatory treatment effects between 13 treated and 13 untreated MS patients. In addition, the expression pattern of 1109 gene transcripts that were previously reported to significantly differentiate between MS patients and healthy subjects were further analyzed to study the effect of cytokine-related pathways on disease pathogenesis. When relative gene expression for 26 MS patients was compared to 18 healthy controls, 30 genes related to various cytokine-associated pathways were identified. These genes belong to a variety of families such as interleukins, small inducible cytokine subfamily and tumor necrosis factor ligand and receptor. Further analysis disclosed seven cytokine-associated genes within the immunomodulatory treatment signature, and two cytokine-associated genes SCYA4 (small inducible cytokine A4) and FCAR (Fc fragment of IgA, CD89) that were common to both the MS gene expression signature and the immunomodulatory treatment gene expression signature. Our results indicate that cytokine-associated genes are involved in various pathogenic pathways in MS and also related to immunomodulatory treatment effects.
机译：多发性硬化症（MS）是一种中枢神经系统疾病，其中活化的自反应性T细胞侵入血脑屏障并引发炎症反应，导致髓磷脂破坏和轴突丢失。 MS的病因学，与其意外发作相关的机制，跨越数十年的不可预测的临床过程以及随着时间的推移导致残疾的不同进展速度，仍然是一个谜。我们已经在外周血单个核细胞（PBMC）中应用了基因表达微阵列技术，以更好地了解MS的发病机理和更好的靶向治疗方法。发现535个基因的特征可区分13位经治疗的MS患者和13位未经治疗的MS患者的免疫调节治疗效果。此外，进一步分析了以前报道的可显着区分MS患者和健康受试者的1109个基因转录物的表达模式，以研究细胞因子相关途径对疾病发病机理的影响。当将26名MS患者的相对基因表达与18名健康对照进行比较时，发现了30种与各种细胞因子相关途径相关的基因。这些基因属于各种家族，例如白介素，小的诱导型细胞因子亚家族以及肿瘤坏死因子配体和受体。进一步的分析揭示了免疫调节治疗标记中的七个与细胞因子相关的基因，以及两个MS基因表达标记和免疫调节均相同的细胞因子相关基因SCYA4（小诱导型细胞因子A4）和FCAR（IgA的Fc片段，CD89）。治疗基因表达签名。我们的结果表明，与细胞因子相关的基因参与MS的各种致病途径，也与免疫调节作用有关。

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