摘要：SummaryEntamoeba 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 withE. 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. Thein vivotransfer 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 AbstractDisplay OmittedHighlights•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 formationImmunology; Microbiology; Microbiology Parasite
