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

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... e 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.