An essential role for TAK1 in the contact hypersensitivity response

查看全文 作　　者：Yan G [1,2]Zhao;Yunqi [2]Wang;Weidong [1]Hao;Yisong Y [2]Wan

机构地区：[1]Department of Toxicology,School of Public Health,Peking University,Beijing,China;[2]Department of Microbiology and Immunology,Lineberger Comprehensive Cancer Center,University of North Carolina at Chapel Hill,NC,USA

出　　处：《Cellular & Molecular Immunology》索引2011年第8卷第4期,共10页

基　　金：the National Institutes of Health(R00AI072956 to YYW);the Beijing Natural Science Foundation(7082054);the National Science and Technology Major Specific Project of the People’s Republic of China(2009ZX09301-010 to WH)and the China Scholarship Council(YGZ). 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-b-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)-c 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. 关键词：CHS DC 2,4-dinitrofluorobenzene(DNFB) TAK1

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An essential role for TAK1 in the contact hypersensitivity response

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