中国科学院机构知识库网格
Chinese Academy of Sciences Institutional Repositories Grid
Transcription of Il17 and Il17f Is Controlled by Conserved Noncoding Sequence 2

文献类型:期刊论文

作者Wang, Xiaohu1; Zhang, Yibing1,2; Yang, Xuexian O.1; Nurieva, Roza I.1; Chang, Seon Hee1; Ojeda, Sandra S.1; Kang, Hong S.3; Schluns, Kimberly S.1; Gui, Jianfang2; Jetten, Anton M.3
刊名IMMUNITY
出版日期2012-01-27
卷号36期号:1页码:23-31
ISSN号1074-7613
通讯作者Dong, C (reprint author), Univ Texas MD Anderson Canc Ctr, Dept Immunol, Houston, TX 77030 USA
中文摘要T helper 17 (Th17) cells specifically transcribe the Il17 and Il17f genes, which are localized in the same chromosome region, but the underlying mechanism is unclear. Here, we report a cis element that we previously named conserved noncoding sequence 2 (CNS2) physically interacted with both Il17 and Il17f gene promoters and was sufficient for regulating their selective transcription in Th17 cells. Targeted deletion of CNS2 resulted in impaired retinoic acid-related orphan receptor gammat (ROR gamma t)-driven IL-17 expression in vitro. CNS2-deficient T cells also produced substantially decreased amounts of IL-17F. These cytokine defects were associated with defective chromatin remodeling in the Ild17-Il17f gene locus, possibly because of effects on CNS2-mediated recruitment of histone-modifying enzymes p300 and JmjC domain-containing protein 3 (JMJD3). CNS2-deficient animals were also shown to be resistant to experimental autoimmune encephalomyelitis (EAE). Our results thus suggest that CNS2 is sufficient and necessary for Il17 and optimal Il17f gene transcription in Th17 cells.
英文摘要T helper 17 (Th17) cells specifically transcribe the Il17 and Il17f genes, which are localized in the same chromosome region, but the underlying mechanism is unclear. Here, we report a cis element that we previously named conserved noncoding sequence 2 (CNS2) physically interacted with both Il17 and Il17f gene promoters and was sufficient for regulating their selective transcription in Th17 cells. Targeted deletion of CNS2 resulted in impaired retinoic acid-related orphan receptor gammat (ROR gamma t)-driven IL-17 expression in vitro. CNS2-deficient T cells also produced substantially decreased amounts of IL-17F. These cytokine defects were associated with defective chromatin remodeling in the Ild17-Il17f gene locus, possibly because of effects on CNS2-mediated recruitment of histone-modifying enzymes p300 and JmjC domain-containing protein 3 (JMJD3). CNS2-deficient animals were also shown to be resistant to experimental autoimmune encephalomyelitis (EAE). Our results thus suggest that CNS2 is sufficient and necessary for Il17 and optimal Il17f gene transcription in Th17 cells.
WOS标题词Science & Technology ; Life Sciences & Biomedicine
类目[WOS]Immunology
研究领域[WOS]Immunology
关键词[WOS]EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS ; RANGE INTRACHROMOSOMAL INTERACTIONS ; CD4(+) T-CELLS ; ROR-GAMMA-T ; NUCLEAR RECEPTORS ; GENE-EXPRESSION ; DIFFERENTIATION ; CYTOKINE ; LOCUS ; LINEAGE
收录类别SCI
资助信息NIH; American Heart Association; 973 National Basic Research Program of China[2010CB126301]; National Multiple Sclerosis Society; Chinese Academy of Sciences; MD Anderson Cancer Center; Leukemia and Lymphoma Society
语种英语
WOS记录号WOS:000299766000007
公开日期2012-04-01
源URL[http://ir.ihb.ac.cn/handle/342005/16731]  
专题水生生物研究所_鱼类生物学及渔业生物技术研究中心_期刊论文
作者单位1.Univ Texas MD Anderson Canc Ctr, Dept Immunol, Houston, TX 77030 USA
2.Chinese Acad Sci, Inst Hydrobiol, State Key Lab Freshwater Ecol & Biotechnol, Wuhan 430072, Peoples R China
3.NIEHS, Cell Biol Sect, LRB, NIH, Res Triangle Pk, NC 27709 USA
推荐引用方式
GB/T 7714
Wang, Xiaohu,Zhang, Yibing,Yang, Xuexian O.,et al. Transcription of Il17 and Il17f Is Controlled by Conserved Noncoding Sequence 2[J]. IMMUNITY,2012,36(1):23-31.
APA Wang, Xiaohu.,Zhang, Yibing.,Yang, Xuexian O..,Nurieva, Roza I..,Chang, Seon Hee.,...&Dong, Chen.(2012).Transcription of Il17 and Il17f Is Controlled by Conserved Noncoding Sequence 2.IMMUNITY,36(1),23-31.
MLA Wang, Xiaohu,et al."Transcription of Il17 and Il17f Is Controlled by Conserved Noncoding Sequence 2".IMMUNITY 36.1(2012):23-31.

入库方式: OAI收割

来源:水生生物研究所

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