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 (γ_c)^−/− 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.

Entamoeba histolytica，一种人类大肠腔内的原生动物寄生虫，偶尔会扩散到肝脏，并引起阿米巴肝脓肿（ALA）。溶组织性大肠杆菌感染后，在感染后早期在肝脏中诱导了高水平的2型细胞因子。但是，这些初始的2型细胞因子在ALA形成中的来源和功能仍不清楚。在这项研究中，我们检查了第2组先天淋巴样细胞（ILC2s）在ALA形成中的作用。肝ILC2数量显着增加，并产生稳定的IL-5水平。的体内ILC2s的转移入的Rag2 ^{- / -}共同γ链（γ _Ç）^{- / -}KO小鼠加重了ALA的形成并伴有嗜酸性粒细胞增多和嗜中性粒细胞减少。此外，IL-33缺陷小鼠和IL-5中和小鼠的ALA形成较少。这些结果表明，ILC2通过产生早期的2型细胞因子并促进嗜酸性粒细胞和嗜中性粒细胞在肝脏中的积累而有助于加剧ALA的发病机理。