Innate lymphoid cells regulate intestinal epithelial cell glycosylation.

نویسندگان

  • Yoshiyuki Goto
  • Takashi Obata
  • Jun Kunisawa
  • Shintaro Sato
  • Ivaylo I Ivanov
  • Aayam Lamichhane
  • Natsumi Takeyama
  • Mariko Kamioka
  • Mitsuo Sakamoto
  • Takahiro Matsuki
  • Hiromi Setoyama
  • Akemi Imaoka
  • Satoshi Uematsu
  • Shizuo Akira
  • Steven E Domino
  • Paulina Kulig
  • Burkhard Becher
  • Jean-Christophe Renauld
  • Chihiro Sasakawa
  • Yoshinori Umesaki
  • Yoshimi Benno
  • Hiroshi Kiyono
چکیده

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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عنوان ژورنال:
  • Science

دوره 345 6202  شماره 

صفحات  -

تاریخ انتشار 2014