Objective: Activation of brown adipose tissue (BAT) has been associated with obesity and metabolic liver diseases including fatty liver. Here, we investigated the role of BAT in regulation of liver fibrosis in mice. Methods: In this study, we checked serum biochemistry and expression levels of fibrotic mediators and inflammatory cytokines in the liver of the mice with liver fibrosis induced by carbon tetrachloride (CCl4) injection for 3 weeks under thermoneutral condition (30℃) or 20℃ temperature. We also investigated the population changes of hepatic immune cells in mice with CCl4-induced liver fibrosis which housed under thermoneutral condition or room temperature. Results: Serum levels of liver injury markers and cholesterols were significantly increased in mice housed under thermoneutral temperature. The expression of Col1a1, Acta2 and inflammatory cytokines including Il1b and Il6 were remarkably upregulated in the liver of mice in thermoneutral condition compared to room temperature (20℃). Moreover, inactivation of BAT by thermoneutrality aggravated hepatic collagen deposition as well as promoted the activation of hepatic stellate cells during CCl4-induced liver fibrogenesis. In consistent with these findings, we also found that the population of infiltrating macrophages, neutrophils and proinflammatory cytokine-producing T cells was significantly increased in the liver of mice with liver fibrosis under thermoneutral condition compared to room temperature. Conclusion: These results suggest that BAT inactivation by thermoneutrality contributes to the activation of pro-inflammatory and pro-fibrotic pathways in CCl4-induced liver fibrogenesis. Thus, BAT-liver axis may serve as a potential therapeutic target for liver fibrosis.