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miRNA-17-92 通过调节性 T 细胞调控白细胞介素-10 的产生并控制实验性自身免疫性脑脊髓炎。

microRNA-17-92 regulates IL-10 production by regulatory T cells and control of experimental autoimmune encephalomyelitis.

机构信息

Diabetes Center and Department of Medicine, University of California San Francisco, San Francisco, CA 94143, USA.

出版信息

J Immunol. 2013 Aug 15;191(4):1594-605. doi: 10.4049/jimmunol.1203567. Epub 2013 Jul 15.

DOI:10.4049/jimmunol.1203567
PMID:23858035
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4160833/
Abstract

microRNAs (miRNA) are essential for regulatory T cell (Treg) function but little is known about the functional relevance of individual miRNA loci. We identified the miR-17-92 cluster as CD28 costimulation dependent, suggesting that it may be key for Treg development and function. Although overall immune homeostasis was maintained in mice with miR-17-92-deficient Tregs, expression of the miR-17-92 miRNA cluster was critical for Treg accumulation and function during an acute organ-specific autoimmune disease in vivo. Treg-specific loss of miR-17-92 expression resulted in exacerbated experimental autoimmune encephalitis and failure to establish clinical remission. Using peptide-MHC tetramers, we demonstrate that the miR-17-92 cluster was specifically required for the accumulation of activated Ag-specific Treg and for differentiation into IL-10-producing effector Treg.

摘要

微小 RNA（miRNA）对于调节性 T 细胞（Treg）的功能至关重要，但对于单个 miRNA 基因座的功能相关性知之甚少。我们发现 miR-17-92 簇依赖于 CD28 共刺激，这表明它可能是 Treg 发育和功能的关键。尽管在 miR-17-92 缺陷型 Treg 小鼠中维持了整体免疫稳态，但在体内急性器官特异性自身免疫性疾病中，miR-17-92 miRNA 簇的表达对于 Treg 的积累和功能至关重要。Treg 特异性缺失 miR-17-92 表达导致实验性自身免疫性脑脊髓炎加重和临床缓解失败。使用肽-MHC 四聚体，我们证明 miR-17-92 簇对于激活的 Ag 特异性 Treg 的积累和分化为产生 IL-10 的效应 Treg 是特异性必需的。

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