Mechanism of Intestinal Homeostasis Regulated by Segmented Filamentous Bacteria and Immune Cells

  • GOTO Yoshiyuki
    Project for Host-Microbial Interactions in Symbiosis and Pathogenesis, Division of Molecular Immunology, Medical Mycology Research Center, Chiba University Division of Mucosal Symbiosis, International Research and Development Center for Mucosal Vaccines, The Institute of Medical Science, The University of Tokyo

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  • SFBによる免疫細胞を介した腸管バリア形成機構の解明
  • 平成27年度日本ビフィズス菌センター研究奨励賞受賞 SFBによる免疫細胞を介した腸管バリア形成機構の解明
  • ヘイセイ 27ネンド ニホン ビフィズスキン センター ケンキュウ ショウレイショウ ジュショウ SFB ニ ヨル メンエキ サイボウ オ カイシタ チョウカン バリア ケイセイ キコウ ノ カイメイ

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The gastrointestinal tract is a unique organ which is constitutively exposed to countless numbers of antigens including commensal bacteria. In order to exclude pathogenic microorganisms and create symbiotic relationships with non-pathogenic bacteria, the host prepares a sophisticated gut immune system. Segmented filamentous bacteria (SFB), a kind of commensal bacteria, have been reported to induce T helper 17 cells (Th17), which are immune cells providing protection against infection by pathogenic bacteria including Citrobacter rodentium. In this study, we examined the detailed mechanisms of the induction of Th17 by SFB. Our results reveal that antigen presentation by dendritic cells (DCs) mediates the induction of Th17 cells, and that the differentiation of Th17 cells is negatively regulated by major histocompatibility complex (MHC) II on group 3 innate lymphoid cells (ILC3). Our results also revealed that SFB are the bacteria responsible for the induction of α1,2-fucose on intestinal epithelial cells. Furthermore, ILC3 are critical inducers of intestinal epithelial α1,2-fucose that is mediated by the production of interleukin 22. α1,2-Fucose on epithelial cells plays a role in protection against infection by pathogenic bacteria such as Salmonella typhimurium. These results unveil a novel function of segmented filamentous bacteria, which not only induce Th17 cells but also induce α1,2-fucose, leading to the establishment of a protective platform against pathogenic microorganisms in rodents.<br>



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