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dc.contributor.author남태규-
dc.date.accessioned2019-01-02T06:21:30Z-
dc.date.available2019-01-02T06:21:30Z-
dc.date.issued2018-05-
dc.identifier.citationSCIENTIFIC REPORTS, v. 8, Article no. 7799en_US
dc.identifier.issn2045-2322-
dc.identifier.urihttps://www.nature.com/articles/s41598-018-26088-y-
dc.identifier.urihttps://repository.hanyang.ac.kr/handle/20.500.11754/81036-
dc.description.abstractCD4(+) T cells are the central for the mammalian adaptive immune system. Naive CD4(+) T cells mainly differentiate in to pro-inflammatory Th1, Th2 and Th17 cells upon antigenic stimulation. IFN-gamma secreting Th1 cells and IL-17 secreting Th17 cells are found to play key roles in autoimmune diseases like multiple sclerosis (MS) and ulcerative colitis (UC). In this study we found NTG-A-009, 6-aminopyridin-3-ol, has great inhibitory effect on in vitro differentiation of Th1 and Th17 cells without affecting regulatory T cells. Moreover, NTG-A-009 had no effect on CD4(+) T cell proliferation and viability. In vivo treatment has shown that NTG-A-009 has ameliorated experimental autoimmune encephalomyelitis (EAE) and dextran sulfate sodium (DSS) induced colitis through the inhibition of Th1 and Th17 cells differentiation. Mechanistically, NTG-A-009 suppressed Th1 and Th17 cells differentiation via the modulation of JAK/STAT signaling pathway. Thus, our data demonstrated that NTG-A-009 ameliorated inflammation through the inhibition of Th1 and Th17 cells generation making it a potential therapeutic candidate for the treatment of inflammatory diseases.en_US
dc.description.sponsorshipThis study was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT & Future Planning of the Korea government (MSIP) (2015R1C1A1A02036328, NRF-2014R1A4A1071040). The funders had no role in study design, collection and analysis of data or preparation of manuscript.en_US
dc.language.isoen_USen_US
dc.publisherNATURE PUBLISHING GROUPen_US
dc.subjectINFLAMMATORY-BOWEL-DISEASEen_US
dc.subjectBLOOD-BRAIN-BARRIERen_US
dc.subjectEFFECTOR T-CELLSen_US
dc.subjectMULTIPLE-SCLEROSISen_US
dc.subjectULCERATIVE-COLITISen_US
dc.subjectCROHNS-DISEASEen_US
dc.subjectIN-VIVOen_US
dc.subjectTRIAMCINOLONE ACETONIDEen_US
dc.subjectSIGNALING PATHWAYen_US
dc.subjectEPITHELIAL-CELLSen_US
dc.titleAmelioration of Experimental autoimmune encephalomyelitis and DSS induced colitis by NTG-A-009 through the inhibition of Th1 and Th17 cells differentiationen_US
dc.typeArticleen_US
dc.relation.no1-
dc.relation.volume8-
dc.identifier.doi10.1038/s41598-018-26088-y-
dc.relation.page7799-7812-
dc.relation.journalSCIENTIFIC REPORTS-
dc.contributor.googleauthorAcharya, Suman-
dc.contributor.googleauthorTimilshina, Maheshwor-
dc.contributor.googleauthorJiang, Liyuan-
dc.contributor.googleauthorNeupane, Sabita-
dc.contributor.googleauthorChoi, Dong-Young-
dc.contributor.googleauthorPark, Sang Won-
dc.contributor.googleauthorLee, Sang Yeul-
dc.contributor.googleauthorJeong, Byeong-Seon-
dc.contributor.googleauthorKim, Jung-Ae-
dc.contributor.googleauthorNam, Tae-Gyu-
dc.contributor.googleauthorChang, Jae-Hoon-
dc.relation.code2018003596-
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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