Gut dysbiosis promotes the breakdown of oral tolerance mediated through dysfunction of mucosal dendritic cells
Summary: While dysbiosis in the gut is implicated in the impaired induction of oral tolerance generated in mesenteric lymph nodes (MesLNs), how dysbiosis affects this process remains unclear. Here, we describe that antibiotic-driven gut dysbiosis causes the dysfunction of CD11c+CD103+ conventional d...
| Main Authors: | , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2023-05-01
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| Series: | Cell Reports |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S2211124723004424 |
| _version_ | 1797838564998774784 |
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| author | Tomohiro Fukaya Tomofumi Uto Shuya Mitoma Hideaki Takagi Yotaro Nishikawa Moe Tominaga Narantsog Choijookhuu Yoshitaka Hishikawa Katsuaki Sato |
| author_facet | Tomohiro Fukaya Tomofumi Uto Shuya Mitoma Hideaki Takagi Yotaro Nishikawa Moe Tominaga Narantsog Choijookhuu Yoshitaka Hishikawa Katsuaki Sato |
| author_sort | Tomohiro Fukaya |
| collection | DOAJ |
| description | Summary: While dysbiosis in the gut is implicated in the impaired induction of oral tolerance generated in mesenteric lymph nodes (MesLNs), how dysbiosis affects this process remains unclear. Here, we describe that antibiotic-driven gut dysbiosis causes the dysfunction of CD11c+CD103+ conventional dendritic cells (cDCs) in MesLNs, preventing the establishment of oral tolerance. Deficiency of CD11c+CD103+ cDCs abrogates the generation of regulatory T cells in MesLNs to establish oral tolerance. Antibiotic treatment triggers the intestinal dysbiosis linked to the impaired generation of colony-stimulating factor 2 (Csf2)-producing group 3 innate lymphoid cells (ILC3s) for regulating the tolerogenesis of CD11c+CD103+ cDCs and the reduced expression of tumor necrosis factor (TNF)-like ligand 1A (TL1A) on CD11c+CD103+ cDCs for generating Csf2-producing ILC3s. Thus, antibiotic-driven intestinal dysbiosis leads to the breakdown of crosstalk between CD11c+CD103+ cDCs and ILC3s for maintaining the tolerogenesis of CD11c+CD103+ cDCs in MesLNs, responsible for the failed establishment of oral tolerance. |
| first_indexed | 2024-04-09T15:42:50Z |
| format | Article |
| id | doaj.art-38c2da20dbf44dcb811415dd6f857515 |
| institution | Directory Open Access Journal |
| issn | 2211-1247 |
| language | English |
| last_indexed | 2024-04-09T15:42:50Z |
| publishDate | 2023-05-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Cell Reports |
| spelling | doaj.art-38c2da20dbf44dcb811415dd6f8575152023-04-27T06:05:48ZengElsevierCell Reports2211-12472023-05-01425112431Gut dysbiosis promotes the breakdown of oral tolerance mediated through dysfunction of mucosal dendritic cellsTomohiro Fukaya0Tomofumi Uto1Shuya Mitoma2Hideaki Takagi3Yotaro Nishikawa4Moe Tominaga5Narantsog Choijookhuu6Yoshitaka Hishikawa7Katsuaki Sato8Division of Immunology, Department of Infectious Diseases, Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki 889-1692, Japan; Japan Agency for Medical Research and Development (AMED), 1-7-1 Otemachi, Chiyoda-ku, Tokyo 100-0004, JapanDivision of Immunology, Department of Infectious Diseases, Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki 889-1692, Japan; Japan Agency for Medical Research and Development (AMED), 1-7-1 Otemachi, Chiyoda-ku, Tokyo 100-0004, JapanDivision of Immunology, Department of Infectious Diseases, Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki 889-1692, Japan; Japan Agency for Medical Research and Development (AMED), 1-7-1 Otemachi, Chiyoda-ku, Tokyo 100-0004, JapanDivision of Immunology, Department of Infectious Diseases, Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki 889-1692, Japan; Japan Agency for Medical Research and Development (AMED), 1-7-1 Otemachi, Chiyoda-ku, Tokyo 100-0004, JapanDivision of Immunology, Department of Infectious Diseases, Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki 889-1692, Japan; Department of Dermatology, Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki 889-1692, JapanDivision of Immunology, Department of Infectious Diseases, Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki 889-1692, Japan; Department of Oral and Maxillofacial Surgery, Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki 889-1692, JapanDivision of Histochemistry and Cell Biology, Department of Anatomy, Faculty of Medicine, University of Miyazaki, Miyazaki 889-1692, JapanDivision of Histochemistry and Cell Biology, Department of Anatomy, Faculty of Medicine, University of Miyazaki, Miyazaki 889-1692, JapanDivision of Immunology, Department of Infectious Diseases, Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki 889-1692, Japan; Japan Agency for Medical Research and Development (AMED), 1-7-1 Otemachi, Chiyoda-ku, Tokyo 100-0004, Japan; Frontier Science Research Center, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki 889-1692, Japan; Corresponding authorSummary: While dysbiosis in the gut is implicated in the impaired induction of oral tolerance generated in mesenteric lymph nodes (MesLNs), how dysbiosis affects this process remains unclear. Here, we describe that antibiotic-driven gut dysbiosis causes the dysfunction of CD11c+CD103+ conventional dendritic cells (cDCs) in MesLNs, preventing the establishment of oral tolerance. Deficiency of CD11c+CD103+ cDCs abrogates the generation of regulatory T cells in MesLNs to establish oral tolerance. Antibiotic treatment triggers the intestinal dysbiosis linked to the impaired generation of colony-stimulating factor 2 (Csf2)-producing group 3 innate lymphoid cells (ILC3s) for regulating the tolerogenesis of CD11c+CD103+ cDCs and the reduced expression of tumor necrosis factor (TNF)-like ligand 1A (TL1A) on CD11c+CD103+ cDCs for generating Csf2-producing ILC3s. Thus, antibiotic-driven intestinal dysbiosis leads to the breakdown of crosstalk between CD11c+CD103+ cDCs and ILC3s for maintaining the tolerogenesis of CD11c+CD103+ cDCs in MesLNs, responsible for the failed establishment of oral tolerance.http://www.sciencedirect.com/science/article/pii/S2211124723004424CP: Immunology |
| spellingShingle | Tomohiro Fukaya Tomofumi Uto Shuya Mitoma Hideaki Takagi Yotaro Nishikawa Moe Tominaga Narantsog Choijookhuu Yoshitaka Hishikawa Katsuaki Sato Gut dysbiosis promotes the breakdown of oral tolerance mediated through dysfunction of mucosal dendritic cells Cell Reports CP: Immunology |
| title | Gut dysbiosis promotes the breakdown of oral tolerance mediated through dysfunction of mucosal dendritic cells |
| title_full | Gut dysbiosis promotes the breakdown of oral tolerance mediated through dysfunction of mucosal dendritic cells |
| title_fullStr | Gut dysbiosis promotes the breakdown of oral tolerance mediated through dysfunction of mucosal dendritic cells |
| title_full_unstemmed | Gut dysbiosis promotes the breakdown of oral tolerance mediated through dysfunction of mucosal dendritic cells |
| title_short | Gut dysbiosis promotes the breakdown of oral tolerance mediated through dysfunction of mucosal dendritic cells |
| title_sort | gut dysbiosis promotes the breakdown of oral tolerance mediated through dysfunction of mucosal dendritic cells |
| topic | CP: Immunology |
| url | http://www.sciencedirect.com/science/article/pii/S2211124723004424 |
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