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dc.contributor.author남태규-
dc.date.accessioned2018-05-31T04:57:43Z-
dc.date.available2018-05-31T04:57:43Z-
dc.date.issued2017-01-
dc.identifier.citationPLOS ONE, v. 12, No. 1, Article no. e0168942en_US
dc.identifier.issn1932-6203-
dc.identifier.urihttp://journals.plos.org/plosone/article?id=10.1371/journal.pone.0168942-
dc.identifier.urihttp://repository.hanyang.ac.kr/handle/20.500.11754/71780-
dc.description.abstractCD4+ T cells are essential in inflammation and autoimmune diseases. Interferon-γ (IFN-γ) secreting T helper (Th1) and IL-17 secreting T helper (Th17) cells are critical for several autoimmune diseases. To assess the inhibitory effect of a given compound on autoimmune disease, we screened many compounds with an in vitro Th differentiation assay. BJ-3105, a 6-alkoxypyridin-3-ol analog, inhibited IFN-γ and IL-17 production from polyclonal CD4+ T cells and ovalbumin (OVA)-specific CD4+ T cells which were activated by T cell receptor (TCR) engagement. BJ-3105 ameliorated the experimental autoimmune encephalomyelitis (EAE) model by reducing Th1 and Th17 generation. Notably, Th cell differentiation was significantly suppressed by BJ-3105 treatment without inhibiting in vitro proliferation of T cells or inducing programmed cell death. Mechanistically, BJ-3105 inhibited the phosphorylation of JAK and its downstream signal transducer and activator of transcription (STAT) that is critical for Th differentiation. These results demonstrated that BJ-3105 inhibits the phosphorylation of STAT in response to cytokine signals and subsequently suppressed the differentiation of Th cell responses.en_US
dc.description.sponsorshipThis work was supported by a Yeungnam University Research Grant, 213A367004, (http://www.yu.ac.kr/index.php). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.en_US
dc.language.isoen_USen_US
dc.publisherPUBLIC LIBRARY SCIENCEen_US
dc.subjectMULTIPLE-SCLEROSISen_US
dc.subjectENCEPHALITOGENIC ANTIGENSen_US
dc.subjectIMMUNE DEVIATIONen_US
dc.subjectTH17 CELLSen_US
dc.subjectIN-VIVOen_US
dc.subjectGM-CSFen_US
dc.subjectCYTOKINESen_US
dc.subjectIL-17en_US
dc.subjectPATHOGENESISen_US
dc.subjectINDUCTIONen_US
dc.titleBJ-3105, a 6-Alkoxypyridin-3-ol Analog, Impairs T Cell Differentiation and Prevents Experimental Autoimmune Encephalomyelitis Disease Progressionen_US
dc.typeArticleen_US
dc.relation.no1-
dc.relation.volume12-
dc.identifier.doi10.1371/journal.pone.0168942-
dc.relation.page168942-168959-
dc.relation.journalPLOS ONE-
dc.contributor.googleauthorTimilshina, Maheshwor-
dc.contributor.googleauthorKang, Youra-
dc.contributor.googleauthorDahal, Ishmit-
dc.contributor.googleauthorYou, Zhiwei-
dc.contributor.googleauthorNam, Tae-gyu-
dc.contributor.googleauthorKim, Keuk-Jun-
dc.contributor.googleauthorJeong, Byeong-Seon-
dc.contributor.googleauthorChang, Jae-Hoon-
dc.relation.code2017006599-
dc.sector.campusE-
dc.sector.daehakCOLLEGE OF PHARMACY[E]-
dc.sector.departmentDEPARTMENT OF PHARMACY-
dc.identifier.pidtnam-
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COLLEGE OF PHARMACY[E](약학대학) > PHARMACY(약학과) > Articles
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