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论文题目: Ash1l and lnc-Smad3 coordinate Smad3 locus accessibility to modulate iTreg polarization and T cell autoimmunity
英文论文题目: Ash1l and lnc-Smad3 coordinate Smad3 locus accessibility to modulate iTreg polarization and T cell autoimmunity
第一作者: Xia, M; Liu, J; Liu, SX; Chen, K; Lin, HY; Jiang, MH; Xu, XQ; Xue, YQ; Liu, W; Gu, Y; Zhang, X; Li, ZQ; Yi, L; Qian, YC; Zhou, C; Li, R; Zhang, X; Li, ZG; Cao, XT
英文第一作者: Xia, M; Liu, J; Liu, SX; Chen, K; Lin, HY; Jiang, MH; Xu, XQ; Xue, YQ; Liu, W; Gu, Y; Zhang, X; Li, ZQ; Yi, L; Qian, YC; Zhou, C; Li, R; Zhang, X; Li, ZG; Cao, XT
联系作者: Cao, XT (reprint author), Chinese Acad Med Sci, Peking Union Med Coll, Dept Immunol, Natl Key Lab Med Mol Biol, Beijing 100005, Peoples R China.
英文联系作者: Cao, XT (reprint author), Chinese Acad Med Sci, Peking Union Med Coll, Dept Immunol, Natl Key Lab Med Mol Biol, Beijing 100005, Peoples R China.
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发表年度: 2017
卷: 8
期:
页码: 15818
摘要: Regulatory T (Treg) cells are important for the maintenance of immune homoeostasis and prevention of autoimmune diseases. Epigenetic modifications have been reported to modulate autoimmunity by altering Treg cell fate. Here we show that the H3K4 methyltransferase Ash1l facilitates TGF-beta-induced Treg cell polarization in vitro and protects mice from T cell-mediated colitis in vivo. Ash1l upregulates Smad3 expression by directly targeting Smad3 promoter to increase local H3K4 trimethylation. Furthermore, we identify an lncRNA, namely lnc-Smad3, which interacts with the histone deacetylase HDAC1 and silences Smad3 transcription. After TGF-beta stimulation, activated Smad3 suppresses lnc-Smad3 transcription, thereby recovering the Smad3 promoter accessibility to Ash1l. By revealing the opposite regulatory functions of Ash1l and lnc-Smad3 in Smad3 expression, our data provide insights for the epigenetic control of Treg cell fate to potentially aid in the development of therapeutic intervention for autoimmune diseases.
英文摘要: Regulatory T (Treg) cells are important for the maintenance of immune homoeostasis and prevention of autoimmune diseases. Epigenetic modifications have been reported to modulate autoimmunity by altering Treg cell fate. Here we show that the H3K4 methyltransferase Ash1l facilitates TGF-beta-induced Treg cell polarization in vitro and protects mice from T cell-mediated colitis in vivo. Ash1l upregulates Smad3 expression by directly targeting Smad3 promoter to increase local H3K4 trimethylation. Furthermore, we identify an lncRNA, namely lnc-Smad3, which interacts with the histone deacetylase HDAC1 and silences Smad3 transcription. After TGF-beta stimulation, activated Smad3 suppresses lnc-Smad3 transcription, thereby recovering the Smad3 promoter accessibility to Ash1l. By revealing the opposite regulatory functions of Ash1l and lnc-Smad3 in Smad3 expression, our data provide insights for the epigenetic control of Treg cell fate to potentially aid in the development of therapeutic intervention for autoimmune diseases.
刊物名称: NATURE COMMUNICATIONS
英文刊物名称: NATURE COMMUNICATIONS
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学科: Multidisciplinary Sciences
英文学科: Multidisciplinary Sciences
影响因子: 12.124
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论文类别: Article
英文论文类别: Article
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