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X-tra X: An escape to autoimmunity

机译:X-tra X:逃避自身免疫

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摘要

Identifying the factors driving disease disparities between males and females with multiple sclerosis (MS) holds great promise for deciphering immunopathogenic disease mechanisms. In this issue of JCI, Itoh et al. explore the basis for sexual dimorphism in autoimmunity, specifically in MS. Using the experimental autoimmune encephalomyelitis (EAE) model of MS, which recapitulates CD4+ T cell-dependent disease, the authors examined the contribution of Kdm6a, a histone demethylase gene known to escape X inactivation. Conditional knockout in CD4+ T cells revealed Kdm6a involvement with a collection of immunologic processes having the potential to skew immunity toward inflammatory responses. This study concisely shows the value of X chromosome gene expression in T cell regulation of autoimmunity and the relevance of Kdm6a in the pathogenesis of EAE as a model of MS.
机译:确定导致多发性硬化症 (MS) 男性和女性之间疾病差异的因素对于破译免疫致病性疾病机制具有很大希望。在本期JCI中,Itoh等人探讨了自身免疫中性二态性的基础,特别是在MS中。 使用MS的实验性自身免疫性脑脊髓炎(EAE)模型,该模型概括了CD4 + T细胞依赖性疾病,作者检查了Kdm6a的贡献,Kdm6a是一种已知可以逃避X失活的组蛋白去甲基化酶基因。CD4+ T 细胞的条件敲除显示 Kdm6a 参与一系列免疫过程,这些过程有可能使免疫力偏向炎症反应。本研究简明扼要地揭示了X染色体基因表达在T细胞调节自身免疫中的价值,以及Kdm6a作为MS模型在EAE发病机制中的相关性。

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