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An essential role for TAK1 in the contact hypersensitivity response
Zhao, Yan G.1,2; Wang, Yunqi1; Hao, Weidong2; Wan, Yisong Y.1
关键词Chs Dc Tak1 2 4-dinitrofluorobenzene (Dnfb)
刊名CELLULAR & MOLECULAR IMMUNOLOGY
2011-07-01
DOI10.1038/cmi.2011.11
8期:4页:315-324
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Immunology
研究领域[WOS]Immunology
关键词[WOS]NF-KAPPA-B ; CD8(+) T-CELLS ; ADAPTIVE IMMUNE-RESPONSES ; KINASE TAK1 ; KERATINOCYTE APOPTOSIS ; RHEUMATOID-ARTHRITIS ; SKIN INFLAMMATION ; EFFECTOR-CELLS ; TGF-BETA ; DERMATITIS
英文摘要

Contact hypersensitivity (CHS) is a delayed-type hypersensitivity that can be induced by haptens, such as 2,4-dinitrofluorobenzene (DNFB). Innate and adaptive immunities are both important for the development of CHS. To treat CHS-related diseases, such as allergic contact dermatitis, a disease prevalent in industrialized countries, ways of interfering with improper immune function during CHS responses need to be identified. Transforming growth factor-beta-activated kinase-1 (TAK1), a member of mitogen-activated protein kinase kinase kinase family, is important for both innate and adaptive immunities. We thus hypothesized that the CHS response could be inhibited by interfering with TAK1 activity. Using a mouse model in which TAK1 deletion can be locally induced, we observed that TAK deficiency led to an impaired CHS response and was associated with defective T-cell expansion, activation and interferon (IFN)-gamma production. In addition, we investigated the effect of deleting TAK1 specifically in dendritic cells (DC) on the CHS response. We found that when TAK1 is deficient in DC, the CHS response was abolished and hapten-elicited T-cell responses were defective. Collectively, this study demonstrates an essential role of TAK1 in the induction of CHS and suggests that targeting TAK1 could be a viable approach to treat CHS. Cellular & Molecular Immunology (2011) 8, 315-324; doi: 10.1038/cmi.2011.11; published online 9 May 2011

语种英语
WOS记录号WOS:000292320800006
项目编号R00AI072956 ; 7082054 ; 2009ZX09301-010
资助机构National Institutes of Health ; Beijing Natural Science Foundation ; National Science and Technology Major Specific Project of the People&prime ; s Republic of China ; China Scholarship Council
引用统计
被引频次:9[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/52015
专题北京大学公共卫生学院_毒理学系
作者单位1.Univ N Carolina, Dept Microbiol & Immunol, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA
2.Peking Univ, Sch Publ Hlth, Dept Toxicol, Beijing 100191, Peoples R China
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GB/T 7714
Zhao, Yan G.,Wang, Yunqi,Hao, Weidong,et al. An essential role for TAK1 in the contact hypersensitivity response[J]. CELLULAR & MOLECULAR IMMUNOLOGY,2011,8(4):315-324.
APA Zhao, Yan G.,Wang, Yunqi,Hao, Weidong,&Wan, Yisong Y..(2011).An essential role for TAK1 in the contact hypersensitivity response.CELLULAR & MOLECULAR IMMUNOLOGY,8(4),315-324.
MLA Zhao, Yan G.,et al."An essential role for TAK1 in the contact hypersensitivity response".CELLULAR & MOLECULAR IMMUNOLOGY 8.4(2011):315-324.
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