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Summary Entamoeba histolytica, a protozoan parasite in the lumen of the human large intestine, occasionally spreads to the liver and induces amebic liver abscesses (ALAs). Upon infection with E. histolytica, high levels of type 2 cytokines are induced in the liver early after infection. However, the sources and functions of these initial type 2 cytokines in ALA formation remain unclear. In this study, we examined the roles of group 2 innate lymphoid cells (ILC2s) in ALA formation. Hepatic ILC2 numbers were significantly increased and they produced robust levels of IL-5. The in vivo transfer of ILC2s into Rag2−/−common γ chain (γc)−/− KO mice aggravated ALA formation accompanied by eosinophilia and neutrophilia. Furthermore, IL-33-deficient mice and IL-5-neutralized mice had less ALA formations. These results suggest that ILC2s contribute to exacerbating the pathogenesis of ALA by producing early type 2 cytokines and promoting the accumulation of eosinophils and neutrophils in the liver., Graphical Abstract, Highlights • ILC2s exacerbate ALA by promoting the accumulation of eosinophils and neutrophils • Hepatic ILC2s are increased and the main source of IL-5 in the early phase of ALA • Hepatic ILC2s localize with IL-33+ cells in the inflammatory areas of ALA • IL-33 is a trigger of ILC2-mediated ALA formation, Immunology; Microbiology; Microbiology Parasite