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Cited 60 time in webofscience Cited 63 time in scopus
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dc.contributor.authorMoon, SJ-
dc.contributor.authorPark, JS-
dc.contributor.authorHeo, YJ-
dc.contributor.authorKang, CM-
dc.contributor.authorKim, EK-
dc.contributor.authorLim, MA-
dc.contributor.authorRyu, JG-
dc.contributor.authorPark, SJ-
dc.contributor.authorPark, KS-
dc.contributor.authorSung, YC-
dc.contributor.authorPark, SH-
dc.contributor.authorKim, HY-
dc.contributor.authorMin, JK-
dc.contributor.authorCho, ML-
dc.date.accessioned2015-06-25T01:56:28Z-
dc.date.available2015-06-25T01:56:28Z-
dc.date.created2015-02-04-
dc.date.issued2013-10-
dc.identifier.issn1226-3613-
dc.identifier.other2015-OAK-0000030973en_US
dc.identifier.urihttps://oasis.postech.ac.kr/handle/2014.oak/10207-
dc.description.abstractInterleukin (IL)-27 is a novel cytokine of the IL-6/IL-12 family that has been reported to be involved in the pathogenesis of autoimmune diseases and has a pivotal role as both a pro-and anti-inflammatory cytokine. We investigated the in vivo effects of IL-27 on arthritis severity in a murine collagen-induced arthritis (CIA) model and its mechanism of action regarding control of regulatory T (Tregs) and IL-17-producing T helper 17 (Th17) cells. IL-27-Fc-treated CIA mice showed a lower severity of arthritis. IL-17 expression in the spleens was significantly decreased in IL-27-Fc-treated CIA mice compared with that in the CIA model. The Th17 population was decreased in the spleens of IL-27-Fc-treated CIA mice, whereas the CD4(+)CD25(+)Foxp(3+) Treg population increased. In vitro studies revealed that IL-27 inhibited IL-17 production in murine CD4(+) T cells, and the effect was associated with retinoic acid-related orphan receptor gamma T and signal transducer and activator of transcription 3 inhibition. In contrast, fluorescein isothiocyanate-labeled forkhead box P3 (Foxp3) and IL-10 were profoundly augmented by IL-27 treatment. Regarding the suppressive capacity of Treg cells, the proportions of CTLA-4(+) (cytotoxic T-lymphocyte antigen 4), PD-1(+) (programmed cell death protein 1) and GITR(+) (glucocorticoid-induced tumor necrosis factor receptor) Tregs increased in the spleens of IL-27-Fc-treated CIA mice. Furthermore, in vitro differentiated Treg cells with IL-27 exerted a more suppressive capacity on T-cell proliferation. We found that IL-27 acts as a reciprocal regulator of the Th17 and Treg populations in CD4(+) cells isolated from healthy human peripheral blood mononuclear cells (PBMCs), as well as from humans with rheumatoid arthritis (RA) PBMCs. Our study suggests that IL-27 has the potential to ameliorate overwhelming inflammation in patients with RA through a reciprocal regulation of Th17 and Treg cells.-
dc.description.statementofresponsibilityopenen_US
dc.languageEnglish-
dc.publisherNATURE PUBLISHING GROUP-
dc.relation.isPartOfEXPERIMENTAL AND MOLECULAR MEDICINE-
dc.rightsBY_NC_NDen_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/2.0/kren_US
dc.subjectcollagen-induced arthritis-
dc.subjectinterleukin-27-
dc.subjectinterleukin-17-producing T cells-
dc.subjectregulatory T cells-
dc.subjectrheumatoid arthritis-
dc.subjectTNF-ALPHA THERAPY-
dc.subjectPATHOGENIC T-CELL-
dc.subjectRHEUMATOID-ARTHRITIS-
dc.subjectDESTRUCTIVE ARTHRITIS-
dc.subjectTGF-BETA-
dc.subjectAUTOIMMUNE ENCEPHALOMYELITIS-
dc.subjectINTERFERON-GAMMA-
dc.subjectSYNOVIAL-FLUID-
dc.subjectANIMAL-MODELS-
dc.subjectINFLAMMATION-
dc.titleIn vivo action of IL-27: reciprocal regulation of Th17 and Treg cells in collagen-induced arthritis-
dc.typeArticle-
dc.contributor.college융합생명공학부en_US
dc.identifier.doi10.1038/EMM.2013.89-
dc.author.googleMoon, SJen_US
dc.author.googlePark, JSen_US
dc.author.googleCho, MLen_US
dc.author.googleMin, JKen_US
dc.author.googleKim, HYen_US
dc.author.googlePark, SHen_US
dc.author.googleSung, YCen_US
dc.author.googlePark, KSen_US
dc.author.googlePark, SJen_US
dc.author.googleRyu, JGen_US
dc.author.googleLim, MAen_US
dc.author.googleKim, EKen_US
dc.author.googleKang, CMen_US
dc.author.googleHeo, YJen_US
dc.relation.volume45en_US
dc.contributor.id10053752en_US
dc.relation.journalEXPERIMENTAL AND MOLECULAR MEDICINEen_US
dc.relation.indexSCI급, SCOPUS 등재논문en_US
dc.relation.sciSCIen_US
dc.collections.nameJournal Papersen_US
dc.type.rimsART-
dc.identifier.bibliographicCitationEXPERIMENTAL AND MOLECULAR MEDICINE, v.45-
dc.identifier.wosid000328123500002-
dc.date.tcdate2019-01-01-
dc.citation.titleEXPERIMENTAL AND MOLECULAR MEDICINE-
dc.citation.volume45-
dc.contributor.affiliatedAuthorSung, YC-
dc.identifier.scopusid2-s2.0-84892421982-
dc.description.journalClass1-
dc.description.journalClass1-
dc.description.wostc33-
dc.description.scptc30*
dc.date.scptcdate2018-10-274*
dc.type.docTypeArticle-
dc.subject.keywordPlusPATHOGENIC T-CELL-
dc.subject.keywordPlusRHEUMATOID-ARTHRITIS-
dc.subject.keywordPlusAUTOIMMUNE ENCEPHALOMYELITIS-
dc.subject.keywordPlusDESTRUCTIVE ARTHRITIS-
dc.subject.keywordPlusTGF-BETA-
dc.subject.keywordPlusDISTINCT-
dc.subject.keywordPlusINFLAMMATION-
dc.subject.keywordPlusINDUCTION-
dc.subject.keywordPlusCTLA-4-
dc.subject.keywordPlusALPHA-
dc.subject.keywordAuthorcollagen-induced arthritis-
dc.subject.keywordAuthorinterleukin-27-
dc.subject.keywordAuthorinterleukin-17-producing T cells-
dc.subject.keywordAuthorregulatory T cells-
dc.subject.keywordAuthorrheumatoid arthritis-
dc.relation.journalWebOfScienceCategoryBiochemistry & Molecular Biology-
dc.relation.journalWebOfScienceCategoryMedicine, Research & Experimental-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.description.journalRegisteredClasskci-
dc.relation.journalResearchAreaBiochemistry & Molecular Biology-
dc.relation.journalResearchAreaResearch & Experimental Medicine-

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