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Innate lymphoid cells regulate intestinal epithelial cell glycosylation

Innate lymphoid cells regulate intestinal epithelial cell glycosylation

Science DOI: 10.1126/science.1254009
Yoshiyuki Goto1,2,3, Takashi Obata1,3, Jun Kunisawa1,4,5, Shintaro Sato1,2, Ivaylo I. Ivanov6, Aayam Lamichhane1, Natsumi Takeyama1, Mariko Kamioka1, Mitsuo Sakamoto3, Takahiro Matsuki7, Hiromi Setoyama7, Akemi Imaoka7, Satoshi Uematsu8,9, Shizuo Akira10, Steven E. Domino11, Paulina Kulig12, Burkhard Becher12, Jean-Christophe Renauld13, Chihiro Sasakawa14,15,16, Yoshinori Umesaki7, Yoshimi Benno17, and Hiroshi Kiyono1,2,5
1 Division of Mucosal Immunology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan 2 Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Saitama 332-0012, Japan 3 Microbe Division/Japan Collection of Microorganisms, RIKEN BioResource Center, Tsukuba 305-0074, Japan 4 Laboratory of Vaccine Materials, National Institute of Biomedical Innovation, Osaka 567-0085, Japan 5 Division of Mucosal Immunology, International Research and Development Center for Mucosal Vaccines, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan 6 Department of Microbiology and Immunology, Columbia University Medical Center, New York, NY 10032 7 Yakult Central Institute for Microbiological Research, Tokyo 186-8650, Japan 8 Division of Innate Immune Regulation, International Research and Development Center for Mucosal Vaccines, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan 9 Department of Mucosal Immunology, School of Medicine, Chiba University, 1-8-1 Inohana, Chuou-ku, Chiba, 260-8670, Japan 10 Laboratory of Host Defense, WPI Immunology Frontier Research Center, Osaka University, Osaka 565-0871, Japan 11 Department of Obstetrics and Gynecology, Cellular and Molecular Biology Program, University of Michigan Medical Center, Ann Arbor, MI 48109-5617 12 Institute of Experimental Immunology, University of Zürich, Winterthurerstrasse 190, Zürich CH-8057, Switzerland 13 Ludwig Institute for Cancer Research and Université Catholique de Louvain, Brussels B-1200, Belgium 14 Division of Bacterial Infection, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan 15 Medical Mycology Research Center, Chiba University, Chiba 260-8673, Japan 16 Nippon Institute for Biological Science, Tokyo 198-0024, Japan 17 Benno Laboratory, Innovation Center, RIKEN, Saitama 351-0198, Japan

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 utilized 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.