期刊
SCIENCE
卷 345, 期 6202, 页码 1310-+出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1254009
关键词
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资金
- Japan Science and Technology Agency
- Ministry of Education, Culture, Sports, Science and Technology of Japan [230000-12]
- Global Center of Excellence (COE) Program Center of Education and Research for Advanced Genome-based Medicine
- Ministry of Health, Labor and Welfare of Japan
- Science and Technology Research Promotion Program for Agriculture, Forestry, Fisheries and Food Industry
- Mochida Memorial Foundation for Medical and Pharmaceutical Research
- National Institutes of Health [1R01DK098378]
- Crohn's and Colitis Foundation of America [259540]
- Grants-in-Aid for Scientific Research [26293111, 23000012] Funding Source: KAKEN
Fucosylation of intestinal epithelial cells, catalyzed by fucosyltransferase 2 (Fut2), is a major glycosylation mechanism of host-microbiota symbiosis. Commensal bacteria induce epithelial fucosylation, and epithelial fucose is used as a dietary carbohydrate by many of these bacteria. However, the molecular and cellular mechanisms that regulate the induction of epithelial fucosylation are unknown. Here, we show that type 3 innate lymphoid cells (ILC3) induced intestinal epithelial Fut2 expression and fucosylation in mice. This induction required the cytokines interleukin-22 and lymphotoxin in a commensal bacteria-dependent and -independent manner, respectively. Disruption of intestinal fucosylation led to increased susceptibility to infection by Salmonella typhimurium. Our data reveal a role for ILC3 in shaping the gut microenvironment through the regulation of epithelial glycosylation.
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