炎症过程中,IL-17信号通过mRNA的内在稳定性控制来调节

IF 0.9 Q4 IMMUNOLOGY AIMS Allergy and Immunology Pub Date : 2022-01-01 DOI:10.3934/allergy.2022014
R. Muromoto, K. Oritani, T. Matsuda
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引用次数: 0

摘要

白细胞介素(IL)-17是一种促炎细胞因子,主要由免疫细胞,特别是活化的t -辅助性17细胞产生,参与银屑病等慢性炎症和自身免疫性疾病的发生。尽管在il -17介导的信号通路中转录的分子机制已经建立,但转录后的控制仍有待阐明。值得注意的是,IL-17调节转录后修饰,诱导目标炎症mrna水平升高。regase -1,一种核糖核酸内切酶和去泛素酶,转录后下调各种il -17驱动的信号通路,包括mRNA的稳定性。il -17刺激可诱导和激活ACT1-TBK1/ ikkλ通路和ARID5A,从而抑制Regnase-1对炎症mRNA的降解。在这篇综述中,我们将重点关注il -17介导的银屑病相关i - κ b -ζ mRNA稳定,并为治疗th17介导的炎症和自身免疫提供新的治疗策略。
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IL-17 signaling is regulated through intrinsic stability control of mRNA during inflammation
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.
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审稿时长
4 weeks
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