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KMID : 0370220180620050297
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Yakhak Hoeji
2018 Volume.62 No. 5 p.297 ~ p.305
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Amelioration of DSS-induced colitis by BJ-2223 through the inhibition of Th17 cell differentiation
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Timilshina Maheshwor
Chang Jae-Hoon
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Abstract
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CD4+ T cells differentiate into T helper (Th) 1 and Th17 cells, which are key mediators of several inflammatory and autoimmune diseases. Inhibition of Th1 and Th17 cell differentiation helps attenuate several inflammatory conditions. Th17 cells are highly pro-inflammatory cells that orchestrate tissue inflammation and ulcerative colitis (UC). Thus, novel compounds that inhibit Th17 cell differentiation are required for the effective treatment of inflammatory and autoimmune diseases. By extensive screening of several synthetic compounds, we found that BJ-2223 inhibits Th17 cell differentiation without affecting Th1 and regulatory T (Treg) cell differentiation in vitro. Furthermore, BJ-2223 does not induce apoptosis and does not affect T cell proliferation and viability. Mechanistically, BJ-2223 inhibits Th17 cell differentiation through inhibition of the Janus-activated kinase (JAK)/signal transducer and activator of transcription protein (STAT) signaling pathway. Moreover, BJ-2223 ameliorates dextran sulfate sodium (DSS)-induced colitis, protects intestinal tissue, and decreases the percentage of Th17 cells in vivo. Thus, BJ-2223 is a novel compound that inhibits in vitro Th17 differentiation and attenuates DSS-induced colitis by reducing the percentage of Th17 cells.
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KEYWORD
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BJ-2223, Th17 cell, Differentiation, JAK/STAT, DSS-induced colitis
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