Interleukin‐33 (IL‐33), the most recently identified member of the IL‐1 family, induces synthesis of T Helper 2 (Th2)‐type cytokines via its heterodimeric ST2/IL‐1RAcP receptor. Th2‐type cytokines play an important role in fibrosis; thus, we investigated the role of IL‐33 in liver fibrosis. IL‐33, ST2 and IL‐1RAcP gene expression was analysed in mouse and human normal (n= 6) and fibrotic livers (n= 28), and in human hepatocellular carcinoma (HCC; n= 22), using real‐time PCR. IL‐33 protein was detected in normal and fibrotic liver sections and in isolated liver cells using Western blotting and immunolocalization approaches. Our results showed that IL‐33 and ST2 mRNA was overproduced in mouse and human fibrotic livers, but not in human HCC. IL‐33 expression correlated with ST2 expression and also with collagen expression in fibrotic livers. The major sources of IL‐33 in normal liver from both mice and human beings are the liver sinusoidal endothelial cells and, in fibrotic liver, the activated hepatic stellate cells (HSC). Moreover, IL‐33 expression was increased in cultured HSC when stimulated by pro‐inflammatory cytokines. In conclusion, IL‐33 is strongly associated with fibrosis in chronic liver injury and activated HSC are a source of IL‐33.