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IRAK 蛋白对固有免疫信号的调节。

Regulation of innate immune signaling by IRAK proteins.

机构信息

Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Chan Medical School, Worcester, MA, United States.

Centro de Tecnologia de Vacinas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil.

出版信息

Front Immunol. 2023 Feb 14;14:1133354. doi: 10.3389/fimmu.2023.1133354. eCollection 2023.

DOI:10.3389/fimmu.2023.1133354
PMID:36865541
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9972678/
Abstract

The Toll-like receptors (TLRs) and interleukin-1 receptors (IL-1R) families are of paramount importance in coordinating the early immune response to pathogens. Signaling most TLRs and IL-1Rs is mediated by the protein myeloid differentiation primary-response protein 88 (MyD88). This signaling adaptor forms the scaffold of the myddosome, a molecular platform that employs IL-1R-associated kinase (IRAK) proteins as main players for transducing signals. These kinases are essential in controlling gene transcription by regulating myddosome assembly, stability, activity and disassembly. Additionally, IRAKs play key roles in other biologically relevant responses such as inflammasome formation and immunometabolism. Here, we summarize some of the key aspects of IRAK biology in innate immunity.

摘要

Toll 样受体 (TLRs) 和白介素-1 受体 (IL-1R) 家族在协调对病原体的早期免疫反应中至关重要。大多数 TLRs 和 IL-1Rs 的信号转导是通过蛋白髓样分化初级反应蛋白 88 (MyD88) 介导的。这种信号转导衔接蛋白形成了 Myddosome 的支架,Myddosome 是一个分子平台,它利用 IL-1R 相关激酶 (IRAK) 蛋白作为主要信号转导因子。这些激酶在通过调节 Myddosome 组装、稳定性、活性和解体来控制基因转录方面至关重要。此外,IRAK 在其他生物学相关反应中也发挥着关键作用,如炎症小体形成和免疫代谢。在这里,我们总结了先天免疫中 IRAK 生物学的一些关键方面。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/315a/9972678/561b1cb0d1fb/fimmu-14-1133354-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/315a/9972678/97815118f2c3/fimmu-14-1133354-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/315a/9972678/ae3b84b46431/fimmu-14-1133354-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/315a/9972678/0cfb3bbd7961/fimmu-14-1133354-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/315a/9972678/723ccd323083/fimmu-14-1133354-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/315a/9972678/561b1cb0d1fb/fimmu-14-1133354-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/315a/9972678/97815118f2c3/fimmu-14-1133354-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/315a/9972678/ae3b84b46431/fimmu-14-1133354-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/315a/9972678/0cfb3bbd7961/fimmu-14-1133354-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/315a/9972678/723ccd323083/fimmu-14-1133354-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/315a/9972678/561b1cb0d1fb/fimmu-14-1133354-g005.jpg

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J Clin Immunol. 2023 Jan;43(1):192-205. doi: 10.1007/s10875-022-01369-4. Epub 2022 Oct 7.
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The IRAK4 scaffold integrates TLR4-driven TRIF and MYD88 signaling pathways.IRAK4 支架整合了 TLR4 驱动的 TRIF 和 MYD88 信号通路。
Cell Rep. 2022 Aug 16;40(7):111225. doi: 10.1016/j.celrep.2022.111225.
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Minimal structure of IRAK-1 to induce degradation of TRAF6.IRAK-1 的最小结构诱导 TRAF6 降解。
Drug Des Devel Ther. 2025 Jul 8;19:5855-5870. doi: 10.2147/DDDT.S526064. eCollection 2025.
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IRAK4 Targeting: A Breakthrough Approach to Combat Hidradenitis Suppurativa.靶向IRAK4:治疗化脓性汗腺炎的突破性方法。
Biologics. 2025 Jun 30;19:387-397. doi: 10.2147/BTT.S525106. eCollection 2025.
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IRAK3 is upregulated in rheumatoid arthritis synovium and delays the onset of experimental arthritis.白细胞介素-1受体相关激酶3(IRAK3)在类风湿性关节炎滑膜中表达上调,并延迟实验性关节炎的发病。
Front Immunol. 2025 Apr 30;16:1468341. doi: 10.3389/fimmu.2025.1468341. eCollection 2025.
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