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IL-17 signaling is regulated through intrinsic stability control of mRNA during inflammation
This item is licensed under:Creative Commons Attribution 4.0 International
| Title: | IL-17 signaling is regulated through intrinsic stability control of mRNA during inflammation |
| Authors: | Muromoto, Ryuta Browse this author →KAKEN DB | | Oritani, Kenji Browse this author →KAKEN DB | | Matsuda, Tadashi Browse this author →KAKEN DB |
| Keywords: | IL-17 | | Th17 | | IκB-ζ | | Regnase-1 | | mRNA stabilization | | inflammation |
| Issue Date: | 26-Sep-2022 |
| Publisher: | AIMS Press |
| Journal Title: | AIMS Allergy and Immunology |
| Volume: | 6 |
| Issue: | 3 |
| Start Page: | 188 |
| End Page: | 199 |
| Publisher DOI: | 10.3934/Allergy.2022014 |
| Abstract: | Interleukin (IL)-17 is a proinflammatory cytokine mainly produced by immune cells, especially activated T-helper 17 cells, which contribute to chronic inflammatory and autoimmune diseases including psoriasis. Although the molecular mechanisms of transcription in IL-17-mediated signaling pathways are well established, post-transcriptional control remains to be elucidated. Notably, IL-17 regulates post-transcriptional modifications, which induce elevated levels of target inflammatory mRNAs. Regnase-1, an endoribonuclease and deubiquitinase, post-transcriptionally downregulates various IL-17-driven signaling pathways, including mRNA stability. The ACT1-TBK1/IKKϵ pathway and ARID5A were induced and activated by IL-17-stimulation, leading to the inhibition of inflammatory mRNA degradation by Regnase-1. In this review, we focus on IL-17-mediated mRNA stabilization of psoriasis-related IκB-ζ and provide novel therapeutic strategies for the treatment of Th17-mediated inflammation and autoimmunity. |
| Rights: | http://creativecommons.org/licenses/by/4.0 |
| Type: | article |
| URI: | http://hdl.handle.net/2115/87701 |
| Appears in Collections: | 薬学研究院 (Faculty of Pharmaceutical Sciences) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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Submitter: 松田 正
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