白细胞介素-17A介导炎症反应与椎间盘退变△（开放获取）

(Open Access) Interleukin-17A mediated inflammatory responses in intervertebral disc degeneration

摘要:

椎间盘退变（intervertebral disc degeneration, IDD） 是引起腰背痛的主要原因之一。IDD 的发病机制复杂，与年龄、创伤、遗传易感性、自身免疫炎症反应等有关。研究表明，白细胞介素在IDD 中扮演着重要的角色，白细胞介素通过介导椎间盘内炎症反应，促进细胞外基质降解以及椎间盘细胞凋亡来加速IDD 的病理过程。白细胞介素-17（interleukin-17, IL-17A） 在退变的椎间盘中高表达，提示其作为一种重要的炎症因子，参与IDD 病理生理过程。IL-17A 通过诱导炎症细胞因子、细胞外基质降解相关因子以及趋化因子等的产生，促进IDD 的发生与发展。本文旨在探讨IL-17A 在椎间盘中的产生与作用以及其介导IDD 发生、发展的分子机制，为防治IDD 提供新思路。

Abstract:

Intervertebral disc degeneration (IDD) is one of the primary causes of low back pain. The pathogenesis of IDD is intricate andinvolves factors such as age, trauma, genetic susceptibility, and autoimmune inflammatory responses. Research indicates that interleukin-17(IL-17A) plays a crucial role in IDD by mediating intra-discal inflammation, promoting extracellular matrix degradation, and accelerating in-tervertebral disc cell apoptosis, thereby expediting the pathological process of IDD. IL-17A is highly expressed in degenerated intervertebraldiscs, suggesting its importance as an inflammatory factor in the pathophysiological processes of IDD. IL-17A induces the production of in-flammatory cytokines, factors related to extracellular matrix degradation, and chemokines, thus promoting the occurrence and developmentof IDD. This article aims to explore the production and function of IL-17A within intervertebral discs and its role in mediating the occur-rence and progression of IDD, offering new insights for the prevention and treatment of IDD.