Toll like receptor 2 knock‐out attenuates carbon tetrachloride (CCl 4 )‐induced liver fibrosis by downregulating MAPK and NF‐κB signaling pathways

Innate immune signaling associated with Toll‐like receptors (TLRs) is a key pathway involved in the progression of liver fibrosis. In this study, we reported that TLR2 is required for hepatic fibrogenesis induced by carbon tetrachloride (CCl 4 ). After CCl 4 treatment, TLR2 −/− mice had reduced liver enzyme levels, diminished collagen deposition, decreased inflammatory infiltration and impaired activation of hepatic stellate cells (HSCs) than wild type (WT) mice. Furthermore, after CCl 4 treatment, TLR2 −/− mice demonstrated downregulated expression of profibrotic and proinflammatory genes and impaired mitogen‐activated protein kinases (MAPK) and nuclear factor kappa B (NF‐κB) activation than WT mice. Collectively, our data indicate that TLR2 deficiency protects against CCl 4 ‐induced liver fibrosis.