 |
English
|
正體中文
|
简体中文
|
全文筆數/總筆數 : 12500/13673 (91%)
造訪人次 : 2589758
線上人數 : 314
|
|
|
資料載入中.....
|
請使用永久網址來引用或連結此文件:
http://ir.nhri.org.tw/handle/3990099045/10010
|
題名: | MicroRNA-17 modulates regulatory T cell function by targeting co-regulators of the foxp3 transcription factor |
作者: | Yang, HY;Barbi, J;Wu, CY;Zheng, Y;Vignali, PDA;Wu, XM;Tao, JH;Park, BV;Bandara, S;Novack, L;Ni, XH;Yang, XP;Chang, KY;Wu, RC;Zhang, JR;Yang, CW;Pardoll, DM;Li, HB;Pan, F |
貢獻者: | National Institute of Cancer Research |
摘要: | Regulatory T (Treg) cells are important in maintaining self-tolerance and immune homeostasis. The Treg cell transcription factor Foxp3 works in concert with other co-regulatory molecules, including Eos, to determine the transcriptional signature and characteristic suppressive phenotype of Treg cells. Here, we report that the inflammatory cytokine interleukin-6 (IL-6) actively repressed Eos expression through microRNA-17 (miR-17). miR-17 expression increased in Treg cells in the presence of IL-6, and its expression negatively correlated with that of Eos. Treg cell suppressive activity was diminished upon overexpression of miR-17 in vitro and in vivo, which was mitigated upon co-expression of an Eos mutant lacking miR-17 target sites. Also, RNAi of miR-17 resulted in enhanced suppressive activity. Ectopic expression of miR-17 imparted effector-T-cell-like characteristics to Treg cells via the derepression of genes encoding effector cytokines. Thus, miR-17 provides a potent layer of Treg cell control through targeting Eos and additional Foxp3 co-regulators. |
日期: | 2016-07-19 |
關聯: | Immunity. 2016 Jul 19;45(1):83-93. |
Link to: | http://dx.doi.org/10.1016/j.immuni.2016.06.022 |
JIF/Ranking 2023: | http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1074-7613&DestApp=IC2JCR |
Cited Times(WOS): | https://www.webofscience.com/wos/woscc/full-record/WOS:000380749000012 |
顯示於類別: | [張光裕] 期刊論文
|
文件中的檔案:
檔案 |
描述 |
大小 | 格式 | 瀏覽次數 |
ISI000380749000012.pdf | | 2618Kb | Adobe PDF | 472 | 檢視/開啟 |
|
在NHRI中所有的資料項目都受到原著作權保護.
|