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Sci Rep. 2018 May 17;8(1):7799. doi: 10.1038/s41598-018-26088-y.

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

Author information

1
College of Pharmacy, Yeungnam University, Gyeongsan, 38541, Republic of Korea.
2
Department of Pharmacy and Institute of Pharmaceutical Science and Technology, Hanyang University, Ansan, 15588, Republic of Korea.
3
Department of Pharmacy and Institute of Pharmaceutical Science and Technology, Hanyang University, Ansan, 15588, Republic of Korea. tnam@hanyang.ac.kr.
4
College of Pharmacy, Yeungnam University, Gyeongsan, 38541, Republic of Korea. jchang@yu.ac.kr.

Abstract

CD4+ T cells are the central for the mammalian adaptive immune system. Naïve CD4+ T cells mainly differentiate in to pro-inflammatory Th1, Th2 and Th17 cells upon antigenic stimulation. IFN-γ 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.

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