中国科学院机构知识库网格
Chinese Academy of Sciences Institutional Repositories Grid
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
出版日期2017
卷号8期号:-页码:15818
ISSN号2041-1723
DOI10.1038/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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