論文 - 詳細
| RRC ID | 86973 |
|---|---|
| 著者 | Yamazaki S, Inohara N, Ohmuraya M, Tsuneoka Y, Yagita H, Katagiri T, Nishina T, Mikami T, Funato H, Araki K, Nakano H. |
| タイトル | IκBζ controls IL-17-triggered gene expression program in intestinal epithelial cells that restricts colonization of SFB and prevents Th17-associated pathologies. |
| ジャーナル | Mucosal Immunol |
| Abstract |
Control of gut microbes is crucial for not only local defense in the intestine but also proper systemic immune responses. Although intestinal epithelial cells (IECs) play important roles in cytokine-mediated control of enterobacteria, the underlying mechanisms are not fully understood. Here we show that deletion of IκBζ in IECs in mice leads to dysbiosis with marked expansion of segmented filamentous bacteria (SFB), thereby enhancing Th17 cell development and exacerbating inflammatory diseases. Mechanistically, the IκBζ deficiency results in decrease in the number of Paneth cells and impairment in expression of IL-17-inducible genes involved in IgA production. The decrease in Paneth cells is caused by aberrant activation of IFN-γ signaling and a failure of IL-17-dependent recovery from IFN-γ-induced damage. Thus, the IL-17R-IκBζ axis in IECs contributes to the maintenance of intestinal homeostasis by serving as a key component in a regulatory loop between the gut microbiota and immune cells. |
| 巻・号 | 15(6) |
| ページ | 1321-1337 |
| 公開日 | 2022-6-1 |
| DOI | 10.1038/s41385-022-00554-3 |
| PII | S1933-0219(22)01757-3 |
| PMID | 35999460 |
| PMC | PMC9705257 |
| MeSH | Adaptor Proteins, Signal Transducing Animals Dysbiosis* / metabolism Epithelial Cells Gene Expression Interleukin-17* / genetics Interleukin-17* / metabolism Intestinal Mucosa Mice Paneth Cells / metabolism Th17 Cells* |
| IF | 6.726 |
| オルトメトリクス指標 |
オルトメトリクス指標項目
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| 最多言及媒体 | X(Twitter) |
| 各媒体での言及数の合計 | 20 |
| 過去6か月間でのオルトメトリクス指標の変動値 | 0.0 |
| リソース情報 | |
| 実験動物マウス | RBRC01834 |