Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 남태규 | - |
dc.date.accessioned | 2019-01-02T06:21:30Z | - |
dc.date.available | 2019-01-02T06:21:30Z | - |
dc.date.issued | 2018-05 | - |
dc.identifier.citation | SCIENTIFIC REPORTS, v. 8, Article no. 7799 | en_US |
dc.identifier.issn | 2045-2322 | - |
dc.identifier.uri | https://www.nature.com/articles/s41598-018-26088-y | - |
dc.identifier.uri | https://repository.hanyang.ac.kr/handle/20.500.11754/81036 | - |
dc.description.abstract | CD4(+) 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.sponsorship | This 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.iso | en_US | en_US |
dc.publisher | NATURE PUBLISHING GROUP | en_US |
dc.subject | INFLAMMATORY-BOWEL-DISEASE | en_US |
dc.subject | BLOOD-BRAIN-BARRIER | en_US |
dc.subject | EFFECTOR T-CELLS | en_US |
dc.subject | MULTIPLE-SCLEROSIS | en_US |
dc.subject | ULCERATIVE-COLITIS | en_US |
dc.subject | CROHNS-DISEASE | en_US |
dc.subject | IN-VIVO | en_US |
dc.subject | TRIAMCINOLONE ACETONIDE | en_US |
dc.subject | SIGNALING PATHWAY | en_US |
dc.subject | EPITHELIAL-CELLS | en_US |
dc.title | Amelioration of Experimental autoimmune encephalomyelitis and DSS induced colitis by NTG-A-009 through the inhibition of Th1 and Th17 cells differentiation | en_US |
dc.type | Article | en_US |
dc.relation.no | 1 | - |
dc.relation.volume | 8 | - |
dc.identifier.doi | 10.1038/s41598-018-26088-y | - |
dc.relation.page | 7799-7812 | - |
dc.relation.journal | SCIENTIFIC REPORTS | - |
dc.contributor.googleauthor | Acharya, Suman | - |
dc.contributor.googleauthor | Timilshina, Maheshwor | - |
dc.contributor.googleauthor | Jiang, Liyuan | - |
dc.contributor.googleauthor | Neupane, Sabita | - |
dc.contributor.googleauthor | Choi, Dong-Young | - |
dc.contributor.googleauthor | Park, Sang Won | - |
dc.contributor.googleauthor | Lee, Sang Yeul | - |
dc.contributor.googleauthor | Jeong, Byeong-Seon | - |
dc.contributor.googleauthor | Kim, Jung-Ae | - |
dc.contributor.googleauthor | Nam, Tae-Gyu | - |
dc.contributor.googleauthor | Chang, Jae-Hoon | - |
dc.relation.code | 2018003596 | - |
dc.sector.campus | E | - |
dc.sector.daehak | COLLEGE OF PHARMACY[E] | - |
dc.sector.department | DEPARTMENT OF PHARMACY | - |
dc.identifier.pid | tnam | - |
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