Type 3 inflammation drives liver fibrosis by enhancing TGF-beta signaling through activation of MAPKS. Type 3 inflammation drives liver fibrosis by enhancing TGF-beta signaling through activation of MAPKS

Type 3 inflammation characterized by increased production of IL-22 is a common driver of liver fibrosis during chronic liver injury through enhancement of TGF-β signaling in a p38 MAPK dependent manner. Overall design: Three lots of human primary hepatitic stellate cells. Each lot was stimulated for 48h with either PBS, TGFlo (0.1ng/mL), TGFhi (2,5ng/mL), IL-17A (40ng/mL), IL-17A + TGFlo, IL-22 (40ng/mL) or IL-22 + TGFlo. Each lot comes from a single donor.