In conclusion, we used mouse models to investigate whether galectins were involved in the immunopathological mechanisms of liver fibrosis caused by S. japonicum infection by blocking galectin-receptor interactions with α-lactose; our data suggested that Gal-3 plays a pivotal role during S. japonicum infection, which leads to attenuated liver functional damage and liver fibrosis by promoting eosinophil infiltration, M1 macrophage polarization, and macrophage autophagy. This evidence concerns the gene LGALS3 and Hepatic fibrosis.