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Transcription factor NFAT1 controls allergic contact hypersensitivity through regulation of activation induced cell death program

DC Field Value Language
dc.contributor.authorHK Kwon-
dc.contributor.authorGi-Cheon Kim-
dc.contributor.authorJi Sun Hwang-
dc.contributor.authorY Kim-
dc.contributor.authorChang-Suk Chae-
dc.contributor.authorJH Nam-
dc.contributor.authorCD Jun-
dc.contributor.authorDipayan Rudra-
dc.contributor.authorCharles D. Surh-
dc.contributor.authorSin-Hyeog Im-
dc.date.available2016-01-28T11:32:38Z-
dc.date.created2016-01-25ko
dc.date.issued2016-01-
dc.identifier.issn2045-2322-
dc.identifier.urihttps://pr.ibs.re.kr/handle/8788114/2372-
dc.description.abstractAllergic contact hypersensitivity (CHS) is an inflammatory skin disease mediated by allergen specific T cells. In this study, we investigated the role of transcription factor NFAT1 in the pathogenesis of contact hypersensitivity. NFAT1 knock out (KO) mice spontaneously developed CHS-like skin inflammation in old age. Healthy young NFAT1 KO mice displayed enhanced susceptibility to hapten-induced CHS. Both CD4+ and CD8+ T cells from NFAT1 KO mice displayed hyper-activated properties and produced significantly enhanced levels of inflammatory T helper 1(Th1)/Th17 type cytokines. NFAT1 KO T cells were more resistant to activation induced cell death (AICD), and regulatory T cells derived from these mice showed a partial defect in their suppressor activity. NFAT1 KO T cells displayed a reduced expression of apoptosis associated BCL-2/BH3 family members. Ectopic expression of NFAT1 restored the AICD defect in NFAT1 KO T cells and increased AICD in normal T cells. Recipient Rag2−/− mice transferred with NFAT1 KO T cells showed more severe CHS sensitivity due to a defect in activation induced hapten-reactive T cell apoptosis. Collectively, our results suggest the NFAT1 plays a pivotal role as a genetic switch in CD4+/CD8+ T cell tolerance by regulating AICD process in the T cell mediated skin inflammation. Copyright © 2016, Macmillan Publishers Limited This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/-
dc.description.uri1-
dc.language영어-
dc.publisherNATURE PUBLISHING GROUP-
dc.titleTranscription factor NFAT1 controls allergic contact hypersensitivity through regulation of activation induced cell death program-
dc.typeArticle-
dc.type.rimsART-
dc.identifier.wosid000391991400001-
dc.identifier.scopusid2-s2.0-84955166662-
dc.identifier.rimsid22239ko
dc.date.tcdate2018-10-01-
dc.contributor.affiliatedAuthorGi-Cheon Kim-
dc.contributor.affiliatedAuthorJi Sun Hwang-
dc.contributor.affiliatedAuthorChang-Suk Chae-
dc.contributor.affiliatedAuthorDipayan Rudra-
dc.contributor.affiliatedAuthorCharles D. Surh-
dc.contributor.affiliatedAuthorSin-Hyeog Im-
dc.identifier.doi10.1038/srep19453-
dc.identifier.bibliographicCitationSCIENTIFIC REPORTS, v.6, pp.19453-
dc.citation.titleSCIENTIFIC REPORTS-
dc.citation.volume6-
dc.citation.startPage19453-
dc.date.scptcdate2018-10-01-
dc.description.wostc4-
dc.description.scptc4-
dc.description.journalClass1-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
Appears in Collections:
Academy of Immunology and Microbiology(면역 미생물 공생 연구단) > 1. Journal Papers (저널논문)
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(2016_GC_Kim)Transcription factor NFAT1 controls allergic contact hypersensitivity through regulation of activation induced cell death program.pdfDownload

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