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BJ-1108, a 6-Amino-2,4,5-trimethylpyridin-3-ol analogue, regulates differentiation of Th1 and Th17 cells to ameliorate experimental autoimmune encephalomyelitis

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
Author
남태규
Keywords
BJ-1108; Th1/Th17 cell; Differentiation; EAE; CENTRAL-NERVOUS-SYSTEM; REMITTING MULTIPLE-SCLEROSIS; EFFECTOR T-CELLS; CYTOKINES; EAE; ANTIOXIDANTS; RESPONSES; BETA; MICE
Issue Date
2017-02
Publisher
SOC BIOLGIA CHILE
Citation
BIOLOGICAL RESEARCH, v. 50, Article no. 8
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.
URI
https://link.springer.com/article/10.1186/s40659-017-0113-zhttp://repository.hanyang.ac.kr/handle/20.500.11754/71692
ISSN
0716-9760; 0717-6287
DOI
10.1186/s40659-017-0113-z
Appears in Collections:
COLLEGE OF PHARMACY[E](약학대학) > PHARMACY(약학과) > Articles
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