Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 남태규 | - |
dc.date.accessioned | 2018-05-31T04:57:43Z | - |
dc.date.available | 2018-05-31T04:57:43Z | - |
dc.date.issued | 2017-01 | - |
dc.identifier.citation | PLOS ONE, v. 12, No. 1, Article no. e0168942 | en_US |
dc.identifier.issn | 1932-6203 | - |
dc.identifier.uri | http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0168942 | - |
dc.identifier.uri | https://repository.hanyang.ac.kr/handle/20.500.11754/71780 | - |
dc.description.abstract | CD4+ 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.sponsorship | This 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.iso | en_US | en_US |
dc.publisher | PUBLIC LIBRARY SCIENCE | en_US |
dc.subject | MULTIPLE-SCLEROSIS | en_US |
dc.subject | ENCEPHALITOGENIC ANTIGENS | en_US |
dc.subject | IMMUNE DEVIATION | en_US |
dc.subject | TH17 CELLS | en_US |
dc.subject | IN-VIVO | en_US |
dc.subject | GM-CSF | en_US |
dc.subject | CYTOKINES | en_US |
dc.subject | IL-17 | en_US |
dc.subject | PATHOGENESIS | en_US |
dc.subject | INDUCTION | en_US |
dc.title | BJ-3105, a 6-Alkoxypyridin-3-ol Analog, Impairs T Cell Differentiation and Prevents Experimental Autoimmune Encephalomyelitis Disease Progression | en_US |
dc.type | Article | en_US |
dc.relation.no | 1 | - |
dc.relation.volume | 12 | - |
dc.identifier.doi | 10.1371/journal.pone.0168942 | - |
dc.relation.page | 168942-168959 | - |
dc.relation.journal | PLOS ONE | - |
dc.contributor.googleauthor | Timilshina, Maheshwor | - |
dc.contributor.googleauthor | Kang, Youra | - |
dc.contributor.googleauthor | Dahal, Ishmit | - |
dc.contributor.googleauthor | You, Zhiwei | - |
dc.contributor.googleauthor | Nam, Tae-gyu | - |
dc.contributor.googleauthor | Kim, Keuk-Jun | - |
dc.contributor.googleauthor | Jeong, Byeong-Seon | - |
dc.contributor.googleauthor | Chang, Jae-Hoon | - |
dc.relation.code | 2017006599 | - |
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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