T cell‐mediated hepatitis is associated with significant morbidity and mortality worldwide. Levels of C‐C chemokine ligand 3/macrophage inflammatory protein‐1α (CCL3/MIP‐1α) are elevated in the serum of patients with T cell‐mediated liver diseases, but its role is not fully understood. Con A‐induced hepatitis is a murine liver‐specific inflammation mediated by activated T cells and is driven by an up‐regulation of the hepatic expression of IFN‐γ. In this study, we have used CCL3/MIP‐1α gene‐deficient mice to examine the role of CCL3/MIP‐1α in the pathogenesis of Con A‐induced hepatitis. We demonstrate a novel pro‐inflammatory role for CCL3/MIP‐1α since CCL3/MIP‐1α deficiency significantly attenuated hepatic injury, both biochemically and histologically. Moreover, the recruitment of CCR1‐expressing CD4⁺ T cells to the liver after Con A treatment was strikingly attenuated by CCL3/MIP‐1α deficiency. Correspondingly, hepatic IFN‐γ produced by the recruited CD4⁺ T cells was significantly reduced by CCL3/MIP‐1α deficiency during Con A‐induced hepatitis. Furthermore, treatment of mice with a dual CCR1/CCR5 peptide antagonist, methionylated RANTES, also markedly reduced hepatic injury and decreased the numbers of CD4⁺ T cells within the liver producing IFN‐γ during Con A‐induced hepatitis. These findings demonstrate that blockade of the CCL3/MIP‐1α‐CCR1 pathway may represent a novel therapeutic target for treating T cell‐mediated liver diseases.