CX3CR1 and Hepatic fibrosis: In contrast, Aoyama et al. reported that whole-body CX3CR1 knockout (CX3CR1−/−) mice exposed to CCl4 exhibited increased inflammatory cell recruitment into the liver and pro-inflammatory cytokine/chemokine production, including TNF-α, IL-1β, CCL2, and CCL5, but decreased expression of anti-inflammatory IL-10 and arginase-1 in Kupffer cells, resulting in enhanced HSC activation and subsequent liver fibrosis [71].