Epithelial glycosylation in gut homeostasis and inflammation
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説明
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.
収録刊行物
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- Nature Immunology
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Nature Immunology 17 (11), 1244-1251, 2016-10-19
Springer Science and Business Media LLC
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キーワード
- Glycosylation
- Polymorphism, Genetic
- Galactoside 2-alpha-L-fucosyltransferase
- Carbohydrates
- Fucosyltransferases
- Immunity, Innate
- Gastroenteritis
- Host-Pathogen Interactions
- Animals
- Carbohydrate Metabolism
- Homeostasis
- Humans
- Genetic Predisposition to Disease
- Lymphocytes
- Intestinal Mucosa
- Immunity, Mucosal
- Fucose
詳細情報 詳細情報について
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- CRID
- 1360846641737777024
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- DOI
- 10.1038/ni.3587
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- ISSN
- 15292916
- 15292908
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- PubMed
- 27760104
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- 資料種別
- journal article
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- データソース種別
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- Crossref
- KAKEN
- OpenAIRE