Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 남태규 | - |
dc.date.accessioned | 2018-05-30T04:21:06Z | - |
dc.date.available | 2018-05-30T04:21:06Z | - |
dc.date.issued | 2017-02 | - |
dc.identifier.citation | BIOLOGICAL RESEARCH, v. 50, Article no. 8 | en_US |
dc.identifier.issn | 0716-9760 | - |
dc.identifier.issn | 0717-6287 | - |
dc.identifier.uri | https://link.springer.com/article/10.1186/s40659-017-0113-z | - |
dc.identifier.uri | https://repository.hanyang.ac.kr/handle/20.500.11754/71692 | - |
dc.description.abstract | Background: CD4(+)T cells play an important role in the initiation of an immune response by providing help to other cells. Among the helper T subsets, interferon-gamma (IFN-gamma)-secreting T helper 1 (Th1) and IL-17-secreting T helper 17 (Th17) cells are indispensable for clearance of intracellular as well as extracellular pathogens. However, Th1 and Th17 cells are also associated with pathogenesis and contribute to the progression of multiple inflammatory conditions and autoimmune diseases. Results: In the current study, we found that BJ-1108, a 6-aminopyridin-3-ol analogue, significantly inhibited Th1 and Th17 differentiation in vitro in a concentration-dependent manner, with no effect on proliferation or apoptosis of activated T cells. Moreover, BJ-1108 inhibited differentiation of Th1 and Th17 cells in ovalbumin (OVA)-specific OT II mice. A complete Freund's adjuvant (CFA)/OVA-induced inflammatory model revealed that BJ-1108 can reduce generation of proinflammatory Th1 and Th17 cells. Furthermore, in vivo studies showed that BJ-1108 delayed onset of disease and suppressed experimental autoimmune encephalomyelitis (EAE) disease progression by inhibiting differentiation of Th1 and Th17 cells. Conclusions: BJ-1108 treatment ameliorates inflammation and EAE by inhibiting Th1 and Th17 cells differentiation. Our findings suggest that BJ-1108 is a promising novel therapeutic agent for the treatment of inflammation and autoimmune disease. | en_US |
dc.description.sponsorship | This work was supported by the Basic Science Research Program from the National Research Foundation of Korea (NRF), funded by the Ministry of Science, ICT & Future Planning of the Korea government (MSIP) (2015R1C1A1A02036328, NRF-2014S1A2A2027903 and NRF-2014R1A4A1071040), and by a Yeungnam University Research Grant. | en_US |
dc.language.iso | en_US | en_US |
dc.publisher | SOC BIOLGIA CHILE | en_US |
dc.subject | BJ-1108 | en_US |
dc.subject | Th1/Th17 cell | en_US |
dc.subject | Differentiation | en_US |
dc.subject | EAE | en_US |
dc.subject | CENTRAL-NERVOUS-SYSTEM | en_US |
dc.subject | REMITTING MULTIPLE-SCLEROSIS | en_US |
dc.subject | EFFECTOR T-CELLS | en_US |
dc.subject | CYTOKINES | en_US |
dc.subject | EAE | en_US |
dc.subject | ANTIOXIDANTS | en_US |
dc.subject | RESPONSES | en_US |
dc.subject | BETA | en_US |
dc.subject | MICE | en_US |
dc.title | BJ-1108, a 6-Amino-2,4,5-trimethylpyridin-3-ol analogue, regulates differentiation of Th1 and Th17 cells to ameliorate experimental autoimmune encephalomyelitis | en_US |
dc.type | Article | en_US |
dc.relation.no | 1 | - |
dc.relation.volume | 50 | - |
dc.identifier.doi | 10.1186/s40659-017-0113-z | - |
dc.relation.page | 8-18 | - |
dc.relation.journal | BIOLOGICAL RESEARCH | - |
dc.contributor.googleauthor | Kang, Youra | - |
dc.contributor.googleauthor | Timilshina, Maheshwor | - |
dc.contributor.googleauthor | Nam, Tae-gyu | - |
dc.contributor.googleauthor | Jeong, Byeong-Seon | - |
dc.contributor.googleauthor | Chang, Jae-Hoon | - |
dc.relation.code | 2017006180 | - |
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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