@article{oai:nagasaki-u.repo.nii.ac.jp:00000082,
 author = {Nakamura, Risa and Yoshizawa, Akihiro and Moriyasu, Taeko and Deloer, Sharmina and Senba, Masachika and Kikuchi, Mihoko and Koyasu, Shigeo and Moro, Kazuyo and Hamano, Shinjiro},
 issue = {9},
 journal = {iScience},
 month = {Sep},
 note = {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., iScience, 23 (9), art.no.101544; 2020},
 title = {Group 2 Innate Lymphoid Cells Exacerbate Amebic Liver Abscess in Mice},
 volume = {23},
 year = {2020}
}