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白细胞介素-25在疾病发病机制中的功能新见解。

New insights into the function of Interleukin-25 in disease pathogenesis.

作者信息

Yuan Qingfang, Peng Na, Xiao Fan, Shi Xiaofei, Zhu Bo, Rui Ke, Tian Jie, Lu Liwei

机构信息

Institute of Medical Immunology, Affiliated Hospital of Jiangsu University, Zhenjiang, China.

Department of Immunology, Jiangsu Key Laboratory of Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, China.

出版信息

Biomark Res. 2023 Apr 1;11(1):36. doi: 10.1186/s40364-023-00474-9.

DOI:10.1186/s40364-023-00474-9
PMID:37005677
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10068183/
Abstract

Interleukin-25 (IL-25), also known as IL-17E, is a cytokine belonging to the IL-17 family. IL-25 is abundantly expressed by Th2 cells and various kinds of epithelial cells. IL-25 is an alarm signal generated upon cell injury or tissue damage to activate immune cells through the interaction with IL-17RA and IL-17RB receptors. The binding of IL-25 to IL-17RA/IL-17RB complex not only initiates and maintains type 2 immunity but also regulates other immune cells (e.g., macrophages and mast cells) via various signaling pathways. It has been well-documented that IL-25 is critically involved in the development of allergic disorders (e.g., asthma). However, the roles of IL-25 in the pathogenesis of other diseases and the underlying mechanisms are still unclear. This review presents current evidence on the roles of IL-25 in cancers, allergic disorders, and autoimmune diseases. Moreover, we discuss the unanswered key questions underlying IL-25-mediated disease pathology, which will provide new insights into the targeted therapy of this cytokine in clinical treatment.

摘要

白细胞介素-25(IL-25),也称为IL-17E,是一种属于IL-17家族的细胞因子。IL-25在Th2细胞和各种上皮细胞中大量表达。IL-25是细胞损伤或组织损伤时产生的一种警报信号,通过与IL-17RA和IL-17RB受体相互作用来激活免疫细胞。IL-25与IL-17RA/IL-17RB复合物的结合不仅启动并维持2型免疫,还通过各种信号通路调节其他免疫细胞(如巨噬细胞和肥大细胞)。已有充分文献证明IL-25在过敏性疾病(如哮喘)的发生发展中起关键作用。然而,IL-25在其他疾病发病机制中的作用及其潜在机制仍不清楚。本综述介绍了关于IL-25在癌症、过敏性疾病和自身免疫性疾病中作用的当前证据。此外,我们讨论了IL-25介导的疾病病理学中尚未解决的关键问题,这将为该细胞因子在临床治疗中的靶向治疗提供新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c41c/10068183/0378185884d4/40364_2023_474_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c41c/10068183/c5c01e5c5ed8/40364_2023_474_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c41c/10068183/73fd4b945ab8/40364_2023_474_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c41c/10068183/6e26c85aa0cd/40364_2023_474_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c41c/10068183/0378185884d4/40364_2023_474_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c41c/10068183/c5c01e5c5ed8/40364_2023_474_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c41c/10068183/73fd4b945ab8/40364_2023_474_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c41c/10068183/6e26c85aa0cd/40364_2023_474_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c41c/10068183/0378185884d4/40364_2023_474_Fig4_HTML.jpg

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