We find IL-19 is upregulated in IPF patients' lung tissues and BLM-induced murine fibrosis models, and the stimulation of lung fibroblasts by IL-19 induces its proliferation and invasion, inhibits apoptosis and promotes its differentiation to myofibroblast phenotype, which can be revised by LY2109761, a TGF-β/Smad signaling pathway inhibitor. Here, TGFB1 is linked to fibrosis.