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10.1126/science.1254009

http://scihub22266oqcxt.onion/10.1126/science.1254009
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C4774895!4774895!25214634
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suck abstract from ncbi


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pmid25214634      Science 2014 ; 345 (6202): 1254009
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  • Innate lymphoid cells regulate intestinal epithelial cell glycosylation #MMPMID25214634
  • Goto Y; Obata T; Kunisawa J; Sato S; Ivanov II; Lamichhane A; Takeyama N; Kamioka M; Sakamoto M; Matsuki T; Setoyama H; Imaoka A; Uematsu S; Akira S; Domino SE; Kulig P; Becher B; Renauld JC; Sasakawa C; Umesaki Y; Benno Y; Kiyono H
  • Science 2014[Sep]; 345 (6202): 1254009 PMID25214634show ga
  • 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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