期刊
ISCIENCE
卷 23, 期 9, 页码 -出版社
CELL PRESS
DOI: 10.1016/j.isci.2020.101544
关键词
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资金
- Japan Society for the Promotion of Science (JSPS) [JP16K19118]
- MEXT [21022037]
- JSPS [23406009, 26305013]
- Grants-in-Aid for Scientific Research [26305013, 23406009, 21022037] Funding Source: KAKEN
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 gamma chain (gamma(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.
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