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首页> 外文期刊>Immunity >MicroRNAs 24 and 27 Suppress Allergic Inflammation and Target a Network of Regulators of T Helper 2 Cell-Associated Cytokine Production
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MicroRNAs 24 and 27 Suppress Allergic Inflammation and Target a Network of Regulators of T Helper 2 Cell-Associated Cytokine Production

机译：MicroRNA 24和27抑制过敏性炎症并针对T辅助2细胞相关细胞因子生产的调节器网络。

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摘要

MicroRNAs (miRNAs) are important regulators of cell fate decisions in immune responses. They act by coordinate repression of multiple target genes, a property that we exploited to uncover regulatory networks that govern T helper-2 (Th2) cells. A functional screen of individual miRNAs in primary T cells uncovered multiple miRNAs that inhibited Th2 cell differentiation. Among these were miR-24 and miR-27, miRNAs coexpressed from two genomic clusters, which each functioned independently to limit interleukin-4 (IL-4) production. Mice lacking both clusters in T cells displayed increased Th2 cell responses and tissue pathology in a mouse model of asthma. Gene expression and pathway analyses placed miR-27 upstream of genes known to regulate Th2 cells. They also identified targets not previously associated with Th2 cell biology which regulated IL-4 production in unbiased functional testing. Thus, elucidating the biological function and target repertoire of miR-24 and miR-27 reveals regulators of Th2 cell biology.
机译：微小RNA（miRNA）是免疫应答中细胞命运决定的重要调节剂。它们通过协调抑制多个靶基因发挥作用，我们利用该特性揭示了控制T辅助2（Th2）细胞的调控网络。在原代T细胞中单个miRNA的功能筛选发现了抑制Th2细胞分化的多个miRNA。其中有miR-24和miR-27，它们是从两个基因组簇共表达的miRNA，每个簇独立发挥功能以限制白介素4（IL-4）的产生。在哮喘小鼠模型中，T细胞缺乏两个簇的小鼠显示出增加的Th2细胞反应和组织病理。基因表达和途径分析将miR-27置于已知可调节Th2细胞的基因的上游。他们还确定了以前与Th2细胞生物学无关的靶标，后者在无偏功能测试中调节了IL-4的产生。因此，阐明miR-24和miR-27的生物学功能和靶标库揭示了Th2细胞生物学的调节剂。

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