microRNA-17-92 regulates IL-10 production by regulatory T cells and control of experimental autoimmune encephalomyelitis.
microRNA-17-92 regulates IL-10 production by regulatory T cells and control of experimental autoimmune encephalomyelitis.
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DOI：
10.4049/jimmunol.1203567
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发表时间：
2013-08-15
期刊：
影响因子：
--
通讯作者：
Jeker LT
中科院分区：
文献类型：
--
作者：
de Kouchkovsky D;Esensten JH;Rosenthal WL;Morar MM;Bluestone JA;Jeker LT
MicroRNAs(MiRNA)是调节性T细胞(Treg)功能所必需的，但人们对单个miRNA基因座的功能相关性知之甚少。我们发现miR-17-92簇是CD28共刺激依赖的，提示它可能是Treg发育和功能的关键。尽管miR-17-92缺乏Treg的小鼠总体上维持了免疫动态平衡，但miR-17-92 miRNA簇的表达对于Treg在体内的急性器官特异性自身免疫性疾病期间的积累和功能至关重要。Treg特异性的miR-17-92表达缺失导致实验性自身免疫性脑炎加重，临床缓解失败。利用肽-MHC四聚体，我们证明了miR-17-92簇是积聚激活的Ag特异性Treg和分化为产生IL-10的效应器Treg所必需的。
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.
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