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Amelioration of Experimental autoimmune encephalomyelitis and DSS induced colitis by NTG-A-009 through the inhibition of Th1 and Th17 cells differentiation

Title
Amelioration of Experimental autoimmune encephalomyelitis and DSS induced colitis by NTG-A-009 through the inhibition of Th1 and Th17 cells differentiation
Author
남태규
Keywords
INFLAMMATORY-BOWEL-DISEASE; BLOOD-BRAIN-BARRIER; EFFECTOR T-CELLS; MULTIPLE-SCLEROSIS; ULCERATIVE-COLITIS; CROHNS-DISEASE; IN-VIVO; TRIAMCINOLONE ACETONIDE; SIGNALING PATHWAY; EPITHELIAL-CELLS
Issue Date
2018-05
Publisher
NATURE PUBLISHING GROUP
Citation
SCIENTIFIC REPORTS, v. 8, Article no. 7799
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.
URI
https://www.nature.com/articles/s41598-018-26088-yhttp://repository.hanyang.ac.kr/handle/20.500.11754/81036
ISSN
2045-2322
DOI
10.1038/s41598-018-26088-y
Appears in Collections:
COLLEGE OF PHARMACY[E](약학대학) > PHARMACY(약학과) > Articles
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