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学科主题基础医学
PDCD5 negatively regulates autoimmunity by upregulating FOXP3(+) regulatory T cells and suppressing Th17 and Th1 responses
Xiao, Juan1,2; Liu, Chen1; Li, Ge1,2; Peng, Saihui1,2; Hu, Jia1,2; Qu, Liujing1,2; Lv, Ping1,2; Zhang, Yu1; Ma, Da Long1,2; Chen, Yingyu1,2
关键词PDCD5 FOXP3 Regulatory T cells Experimental autoimmune encephalomyelitis
刊名JOURNAL OF AUTOIMMUNITY
2013-12-01
DOI10.1016/j.jaut.2013.08.002
47期:0页:34-44
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Immunology
资助者National Key Project for Basic Research of China ; National Natural Science Foundation of China ; 111 Project of China ; National Key Project for Basic Research of China ; National Natural Science Foundation of China ; 111 Project of China
研究领域[WOS]Immunology
关键词[WOS]PROTEIN 5 PDCD5 ; RHEUMATOID-ARTHRITIS ; HISTONE ACETYLTRANSFERASE ; PROGNOSTIC-SIGNIFICANCE ; DISEASE-ACTIVITY ; SYNOVIAL-FLUID ; TUMOR-CELLS ; DNA-DAMAGE ; EXPRESSION ; DEATH
英文摘要

Maintenance of FOXP3 protein expression is crucial for differentiation and maturation of regulatory T (Treg) cells, which play important roles in immune homeostasis and immune tolerance. We demonstrate here that PDCD5 interacts with FOXP3, increases acetylation of FOXP3 in synergy with Tip60 and enhances the repressive function of FOXP3. In PDCD5 transgenic (PDCD5tg) mice, overexpression of PDCD5 enhanced the level of FOXP3 protein and percentage of CD4(+)CD25(+)FOXP3(+) cells. Naive CD4(+) T cells from PDCD5tg mice were more sensitive to TGF-beta-induced Treg polarization and expansion. These induced Tregs retained normal suppressive function in vitro. Severity of experimentally-induced autoimmune encephalomyelitis (EAE) in PDCD5tg mice was significantly reduced relative to that of wild-type mice. The beneficial effect of PDCD5 likely resulted from increases of Treg cell frequency, accompanied by a reduction of the predominant pathogenic Th17/Th1 response. Activation-induced cell death enhanced by PDCD5 was also linked to this process. This is the first report revealing that PDCD5 activity in T cells suppresses autoimmunity by modulating Tregs. This study suggests that PDCD5 serves as a guardian of immunological functions and that the PDCD5-FOXP3-Treg axis may be a therapeutic target for autoimmunity. (C) 2013 Elsevier Ltd. All rights reserved.

语种英语
所属项目编号2011CB910103 ; 2011CB946100 ; 31370898 ; B07001
资助者National Key Project for Basic Research of China ; National Natural Science Foundation of China ; 111 Project of China ; National Key Project for Basic Research of China ; National Natural Science Foundation of China ; 111 Project of China
WOS记录号WOS:000328527100004
引用统计
文献类型期刊论文
版本出版稿
条目标识符http://ir.bjmu.edu.cn/handle/400002259/53495
专题基础医学院_免疫学系
作者单位1.Peking Univ, Hlth Sci Ctr, Key Lab Med Immunol, Minist Hlth, Beijing 100191, Peoples R China
2.Peking Univ, Peking Univ Ctr Human Dis Gen, Beijing 100191, Peoples R China
推荐引用方式
GB/T 7714
Xiao, Juan,Liu, Chen,Li, Ge,et al. PDCD5 negatively regulates autoimmunity by upregulating FOXP3(+) regulatory T cells and suppressing Th17 and Th1 responses[J]. JOURNAL OF AUTOIMMUNITY,2013,47(0):34-44.
APA Xiao, Juan.,Liu, Chen.,Li, Ge.,Peng, Saihui.,Hu, Jia.,...&Chen, Yingyu.(2013).PDCD5 negatively regulates autoimmunity by upregulating FOXP3(+) regulatory T cells and suppressing Th17 and Th1 responses.JOURNAL OF AUTOIMMUNITY,47(0),34-44.
MLA Xiao, Juan,et al."PDCD5 negatively regulates autoimmunity by upregulating FOXP3(+) regulatory T cells and suppressing Th17 and Th1 responses".JOURNAL OF AUTOIMMUNITY 47.0(2013):34-44.
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