title: Epithelial glycosylation in gut homeostasis and inflammation.
abstract: Intestinal epithelial cells apically express glycans, especially α1,2-fucosyl linkages, which work as a biological interface for the host-microbe interaction. Emerging studies have shown that epithelial α1,2-fucosylation is regulated by microbes and by group 3 innate lymphoid cells (ILC3s). Dysregulation of the gene (FUT2) encoding fucosyltransferase 2, an enzyme governing epithelial α1,2-fucosylation, is associated with various human disorders, including infection and chronic inflammatory diseases. This suggests a critical role for an interaction between microbes, epithelial cells and ILC3s mediated via glycan residues. In this Review, using α1,2-fucose and Fut2 gene expression as an example, we describe how epithelial glycosylation is controlled by immune cells and luminal microbes. We also address the pathophysiological contribution of epithelial α1,2-fucosylation to pathogenic and commensal microbes as well as the potential of α1,2-fucose and its regulatory pathway as previously unexploited targets in the development of new therapeutic approaches for human diseases.
authors.affiliation: Division of Molecular Immunology, Medical Mycology Research Center, Chiba University, Chiba, Japan.|International Research and Development Center for Mucosal Vaccines, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Goto
authors.affiliation: International Research and Development Center for Mucosal Vaccines, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.|Department of Mucosal Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
authors.forename: Satoshi
authors.initials: S
authors.lastname: Uematsu
authors.affiliation: International Research and Development Center for Mucosal Vaccines, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.|Department of Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.|Division of Mucosal Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kiyono
mesh_terms: D000818:Animals; D050260:Carbohydrate Metabolism; D002241:Carbohydrates; D005643:Fucose / Q000378:metabolism; D005647:Fucosyltransferases / Q000235:genetics / Q000378:metabolism; D005759:Gastroenteritis / Q000235:genetics / Q000276:immunology / Q000378:metabolism* / Q000382:microbiology; D020022:Genetic Predisposition to Disease; D006031:Glycosylation; D006706:Homeostasis; D054884:Host-Pathogen Interactions / Q000276:immunology; D006801:Humans; D007113:Immunity, Innate; D018928:Immunity, Mucosal; D007413:Intestinal Mucosa / Q000276:immunology / Q000378:metabolism* / Q000382:microbiology; D008214:Lymphocytes / Q000276:immunology / Q000378:metabolism; D011110:Polymorphism, Genetic; D000097631:Galactoside 2-alpha-L-fucosyltransferase
chemical_list: D002241:Carbohydrates; D005643:Fucose; D005647:Fucosyltransferases; D000097631:Galactoside 2-alpha-L-fucosyltransferase