Ash1l and lnc-Smad3 coordinate Smad3 locus accessibility to modulate iTreg polarization and T cell autoimmunity
文献类型:期刊论文
作者 | Xia, Meng7; Jiang, Minghong7; Cao, Xuetao7,8; Liu, Juan8; Liu, Shuxun8; Chen, Kun6; Lin, Hongyu6; Qian, Youcun5; Zhou, Chen2,4; Li, Ru1 |
刊名 | NATURE COMMUNICATIONS
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出版日期 | 2017 |
卷号 | 8期号:-页码:15818 |
ISSN号 | 2041-1723 |
DOI | 10.1038/ncomms15818 |
文献子类 | Article |
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. |
学科主题 | Science & Technology - Other Topics |
WOS关键词 | LONG NONCODING RNA ; EPIGENETIC REGULATION ; FOXP3 EXPRESSION ; GENE-EXPRESSION ; IMMUNE-SYSTEM ; DIFFERENTIATION ; ACTIVATION ; MECHANISMS ; PLASTICITY ; INDUCTION |
语种 | 英语 |
WOS记录号 | WOS:000402985600001 |
出版者 | NATURE PUBLISHING GROUP |
版本 | 出版稿 |
源URL | [http://202.127.25.144/handle/331004/903] ![]() |
专题 | 中国科学院上海生命科学研究院营养科学研究所 |
作者单位 | 1.Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Hlth Sci, Shanghai 200025, Peoples R China; 2.Peking Univ, Peoples Hosp, Dept Rheumatol & Immunol, Beijing 100044, Peoples R China, 3.Chinese Acad Med Sci, Peking Union Med Coll Hosp, Dept Rheumatol, Beijing 100032, Peoples R China; 4.Zhejiang Univ, Inst Immunol, Sch Med, Hangzhou 310058, Zhejiang, Peoples R China; 5.Second Mil Med Univ, Inst Immunol, Shanghai 200433, Peoples R China; 6.Second Mil Med Univ, Natl Key Lab Med Immunol, Shanghai 200433, Peoples R China; 7.Chinese Acad Med Sci, Peking Union Med Coll, Dept Immunol, Natl Key Lab Med Mol Biol, Beijing 100005, Peoples R China; 8.Chinese Acad Med Sci, Peking Union Med Coll, Ctr Immunotherapy, Inst Basic Med Sci, Beijing 100005, Peoples R China; |
推荐引用方式 GB/T 7714 | Xia, Meng,Jiang, Minghong,Cao, Xuetao,et al. Ash1l and lnc-Smad3 coordinate Smad3 locus accessibility to modulate iTreg polarization and T cell autoimmunity[J]. NATURE COMMUNICATIONS,2017,8(-):15818. |
APA | Xia, Meng.,Jiang, Minghong.,Cao, Xuetao.,Liu, Juan.,Liu, Shuxun.,...&,.(2017).Ash1l and lnc-Smad3 coordinate Smad3 locus accessibility to modulate iTreg polarization and T cell autoimmunity.NATURE COMMUNICATIONS,8(-),15818. |
MLA | Xia, Meng,et al."Ash1l and lnc-Smad3 coordinate Smad3 locus accessibility to modulate iTreg polarization and T cell autoimmunity".NATURE COMMUNICATIONS 8.-(2017):15818. |
入库方式: OAI收割
来源:上海营养与健康研究所
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