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dc.contributor.author남태규-
dc.date.accessioned2018-05-30T04:21:06Z-
dc.date.available2018-05-30T04:21:06Z-
dc.date.issued2017-02-
dc.identifier.citationBIOLOGICAL RESEARCH, v. 50, Article no. 8en_US
dc.identifier.issn0716-9760-
dc.identifier.issn0717-6287-
dc.identifier.urihttps://link.springer.com/article/10.1186/s40659-017-0113-z-
dc.identifier.urihttp://repository.hanyang.ac.kr/handle/20.500.11754/71692-
dc.description.abstractBackground: 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.sponsorshipThis 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.isoen_USen_US
dc.publisherSOC BIOLGIA CHILEen_US
dc.subjectBJ-1108en_US
dc.subjectTh1/Th17 cellen_US
dc.subjectDifferentiationen_US
dc.subjectEAEen_US
dc.subjectCENTRAL-NERVOUS-SYSTEMen_US
dc.subjectREMITTING MULTIPLE-SCLEROSISen_US
dc.subjectEFFECTOR T-CELLSen_US
dc.subjectCYTOKINESen_US
dc.subjectEAEen_US
dc.subjectANTIOXIDANTSen_US
dc.subjectRESPONSESen_US
dc.subjectBETAen_US
dc.subjectMICEen_US
dc.titleBJ-1108, a 6-Amino-2,4,5-trimethylpyridin-3-ol analogue, regulates differentiation of Th1 and Th17 cells to ameliorate experimental autoimmune encephalomyelitisen_US
dc.typeArticleen_US
dc.relation.no1-
dc.relation.volume50-
dc.identifier.doi10.1186/s40659-017-0113-z-
dc.relation.page8-18-
dc.relation.journalBIOLOGICAL RESEARCH-
dc.contributor.googleauthorKang, Youra-
dc.contributor.googleauthorTimilshina, Maheshwor-
dc.contributor.googleauthorNam, Tae-gyu-
dc.contributor.googleauthorJeong, Byeong-Seon-
dc.contributor.googleauthorChang, Jae-Hoon-
dc.relation.code2017006180-
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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