Ash1l and lnc-Smad3 coordinate Smad3 locus accessibility to modulate iTreg polarization and T cell autoimmunity

doi:10.1038/s41467-019-09922-3

GSTDTAP > 资源环境科学

DOI	10.1038/s41467-019-09922-3
	Ash1l and lnc-Smad3 coordinate Smad3 locus accessibility to modulate iTreg polarization and T cell autoimmunity
	Xia, Meng 1; Liu, Juan 2; Liu, Shuxun 2; Chen, Kun 3; Lin, Hongyu 3; Jiang, Minghong 1; Xu, Xiaoqing ; Xue, Yiquan ; Liu, Wei ; Gu, Yan ; Zhang, Xiang ; Li, Zhiqing ; Yi, Lin ; Qian, Youcun 4; Zhou, Chen 5,8; Li, Ru 6; Zhang, Xuan 7; Li, Zhanguo ; Cao, Xuetao 1,2
	2019-04-23
发表期刊	NATURE COMMUNICATIONS
ISSN	2041-1723
出版年	2017
卷号	8
文章类型	Article
语种	英语
国家	Peoples R China
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.
领域	资源环境
收录类别	SCI-E
WOS记录号	WOS:000402985600001
WOS关键词	LONG NONCODING RNA ; EPIGENETIC REGULATION ; FOXP3 EXPRESSION ; GENE-EXPRESSION ; IMMUNE-SYSTEM ; DIFFERENTIATION ; ACTIVATION ; MECHANISMS ; PLASTICITY ; INDUCTION
WOS类目	Multidisciplinary Sciences
WOS研究方向	Science & Technology - Other Topics
URL	查看原文
引用统计
文献类型	期刊论文
条目标识符	http://119.78.100.173/C666/handle/2XK7JSWQ/204334
专题	资源环境科学
作者单位	1.Chinese Acad Med Sci, Peking Union Med Coll, Dept Immunol, Natl Key Lab Med Mol Biol, Beijing 100005, Peoples R China; 2.Chinese Acad Med Sci, Peking Union Med Coll, Ctr Immunotherapy, Inst Basic Med Sci, Beijing 100005, Peoples R China; 3.Second Mil Med Univ, Natl Key Lab Med Immunol, Shanghai 200433, Peoples R China; 4.Second Mil Med Univ, Inst Immunol, Shanghai 200433, Peoples R China; 5.Zhejiang Univ, Inst Immunol, Sch Med, Hangzhou 310058, Zhejiang, Peoples R China; 6.Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Hlth Sci, Shanghai 200025, Peoples R China; 7.Chinese Acad Med Sci, Peking Union Med Coll Hosp, Dept Rheumatol, Beijing 100032, Peoples R China; 8.Peking Univ, Peoples Hosp, Dept Rheumatol & Immunol, Beijing 100044, Peoples R China
推荐引用方式 GB/T 7714	Xia, Meng,Liu, Juan,Liu, Shuxun,et al. Ash1l and lnc-Smad3 coordinate Smad3 locus accessibility to modulate iTreg polarization and T cell autoimmunity[J]. NATURE COMMUNICATIONS,2019,8.
APA	Xia, Meng.,Liu, Juan.,Liu, Shuxun.,Chen, Kun.,Lin, Hongyu.,...&Cao, Xuetao.(2019).Ash1l and lnc-Smad3 coordinate Smad3 locus accessibility to modulate iTreg polarization and T cell autoimmunity.NATURE COMMUNICATIONS,8.
MLA	Xia, Meng,et al."Ash1l and lnc-Smad3 coordinate Smad3 locus accessibility to modulate iTreg polarization and T cell autoimmunity".NATURE COMMUNICATIONS 8(2019).