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首页> 外文期刊>Nature immunology >MicroRNA miR-326 regulates TH-17 differentiation and is associated with the pathogenesis of multiple sclerosis.
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MicroRNA miR-326 regulates TH-17 differentiation and is associated with the pathogenesis of multiple sclerosis.

机译：MicroRNA miR-326调节TH-17分化，并与多发性硬化症的发病机理有关。

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摘要

Interleukin 17 (IL-17)-producing T helper cells (T(H)-17 cells) are increasingly recognized as key participants in various autoimmune diseases, including multiple sclerosis. Although sets of transcription factors and cytokines are known to regulate T(H)-17 differentiation, the role of noncoding RNA is poorly understood. Here we identify a T(H)-17 cell-associated microRNA, miR-326, whose expression was highly correlated with disease severity in patients with multiple sclerosis and mice with experimental autoimmune encephalomyelitis (EAE). In vivo silencing of miR-326 resulted in fewer T(H)-17 cells and mild EAE, and its overexpression led to more T(H)-17 cells and severe EAE. We also found that miR-326 promoted T(H)-17 differentiation by targeting Ets-1, a negative regulator of T(H)-17 differentiation. Our data show a critical role for microRNA in T(H)-17 differentiation and the pathogenesis of multiple sclerosis.
机译：产生白介素17（IL-17）的T辅助细胞（T（H）-17细胞）被公认为各种自身免疫性疾病（包括多发性硬化症）的关键参与者。尽管已知转录因子和细胞因子集可调节T（H）-17分化，但对非编码RNA的作用了解甚少。在这里，我们确定了T（H）-17细胞相关的microRNA miR-326，其表达与多发性硬化症患者和实验性自身免疫性脑脊髓炎（EAE）小鼠的疾病严重程度高度相关。 miR-326的体内沉默导致更少的T（H）-17细胞和轻度的EAE，其过表达导致更多的T（H）-17细胞和严重的EAE。我们还发现miR-326通过靶向Ets-1（T（H）-17分化的负调节剂）来促进T（H）-17分化。我们的数据显示microRNA在T（H）-17分化和多发性硬化症的发病机理中的关键作用。

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