IL-17 signaling is regulated through intrinsic stability control of mRNA during inflammation

Author:

Muromoto Ryuta1,Oritani Kenji2,Matsuda Tadashi1

Affiliation:

1. Department of Immunology, Graduate School of Pharmaceutical Sciences Hokkaido University, Kita-Ku Kita 12 Nishi 6, Sapporo 060-0812, Japan

2. Department of Hematology, International University of Health and Welfare, 4-3 Kouzunomori, Narita, Chiba 286-8686, Japan

Abstract

<abstract> <p>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.</p> </abstract>

Publisher

American Institute of Mathematical Sciences (AIMS)

Subject

General Engineering,Energy Engineering and Power Technology

Reference47 articles.

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