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长链非编码 RNA MIAT 作为人类 Th17 细胞分化的调控因子。

Long Intergenic Noncoding RNA MIAT as a Regulator of Human Th17 Cell Differentiation.

机构信息

Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland.

InFLAMES Research Flagship Center , University of Turku, Turku, Finland.

出版信息

Front Immunol. 2022 Jun 15;13:856762. doi: 10.3389/fimmu.2022.856762. eCollection 2022.

DOI:10.3389/fimmu.2022.856762
PMID:35784351
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9242727/
Abstract

T helper 17 (Th17) cells protect against fungal and bacterial infections and are implicated in autoimmunity. Several long intergenic noncoding RNAs (lincRNA) are induced during Th17 differentiation, however, their contribution to Th17 differentiation is poorly understood. We aimed to characterize the function of the lincRNA Myocardial Infarction Associated Transcript (MIAT) during early human Th17 cell differentiation. We found MIAT to be upregulated early after induction of human Th17 cell differentiation along with an increase in the chromatin accessibility at the gene locus. STAT3, a key regulator of Th17 differentiation, directly bound to the MIAT promoter and induced its expression during the early stages of Th17 cell differentiation. MIAT resides in the nucleus and regulates the expression of several key Th17 genes, including IL17A, IL17F, CCR6 and CXCL13, possibly by altering the chromatin accessibility of key loci, including IL17A locus. Further, MIAT regulates the expression of protein kinase C alpha (PKCα), an upstream regulator of IL17A. A reanalysis of published single-cell RNA-seq data showed that MIAT was expressed in T cells from the synovium of RA patients. Our results demonstrate that MIAT contributes to human Th17 differentiation by upregulating several genes implicated in Th17 differentiation. High MIAT expression in T cells of RA patient synovia suggests a possible role of MIAT in Th17 mediated autoimmune pathologies.

摘要

辅助性 T 细胞 17（Th17）细胞可预防真菌感染和细菌感染，并与自身免疫有关。在 Th17 分化过程中会诱导几种长链非编码 RNA（lncRNA），然而，它们对 Th17 分化的贡献尚不清楚。我们旨在研究 lncRNA 心肌梗塞相关转录物（MIAT）在早期人 Th17 细胞分化中的功能。我们发现，MIAT 在人 Th17 细胞分化诱导后早期上调，同时基因座处的染色质可及性增加。STAT3 是 Th17 分化的关键调节因子，直接与 MIAT 启动子结合，并在 Th17 细胞分化的早期诱导其表达。MIAT 位于细胞核内，调节包括 IL17A、IL17F、CCR6 和 CXCL13 在内的几个关键 Th17 基因的表达，可能通过改变包括 IL17A 基因座在内的关键基因座的染色质可及性来实现。此外，MIAT 调节蛋白激酶 Cα（PKCα）的表达，PKCα 是 IL17A 的上游调节因子。对已发表的单细胞 RNA-seq 数据的重新分析表明，MIAT 在 RA 患者滑膜中的 T 细胞中表达。我们的研究结果表明，MIAT 通过上调几个与 Th17 分化相关的基因来促进人 Th17 分化。RA 患者滑膜 T 细胞中高表达 MIAT 提示 MIAT 可能在 Th17 介导的自身免疫病理中发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d3b/9242727/5ac5b47ca5e3/fimmu-13-856762-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d3b/9242727/f418724a1ae0/fimmu-13-856762-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d3b/9242727/4d6bb0d29899/fimmu-13-856762-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d3b/9242727/73c2ec807d84/fimmu-13-856762-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d3b/9242727/e15fd8c6174f/fimmu-13-856762-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d3b/9242727/3f9d2bc7f264/fimmu-13-856762-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d3b/9242727/5ac5b47ca5e3/fimmu-13-856762-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d3b/9242727/f418724a1ae0/fimmu-13-856762-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d3b/9242727/4d6bb0d29899/fimmu-13-856762-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d3b/9242727/73c2ec807d84/fimmu-13-856762-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d3b/9242727/e15fd8c6174f/fimmu-13-856762-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d3b/9242727/3f9d2bc7f264/fimmu-13-856762-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d3b/9242727/5ac5b47ca5e3/fimmu-13-856762-g006.jpg

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