Student Scientific Group of Adult Allergology, Wroclaw Medical University, 50-369 Wroclaw, Poland.
Clinical Department of Internal Medicine, Pneumology and Allergology, Wroclaw Medical University, 50-369 Wroclaw, Poland.
Int J Mol Sci. 2023 Jun 15;24(12):10172. doi: 10.3390/ijms241210172.
Interleukin-23 (IL-23) is a proinflammatory cytokine produced mainly by macrophages and antigen-presenting cells (APCs) after antigenic stimulation. IL-23 plays a significant role as a mediator of tissue damage. Indeed, the irregularities in IL-23 and its receptor signaling have been implicated in inflammatory bowel disease. IL-23 interacts with both the innate and adaptive immune systems, and IL-23/Th17 appears to be involved in the development of chronic intestinal inflammation. The IL-23/Th17 axis may be a critical driver of this chronic inflammation. This review summarizes the main aspects of IL-23's biological function, cytokines that control cytokine production, effectors of the IL-23 response, and the molecular mechanisms associated with IBD pathogenesis. Although IL-23 modulates and impacts the development, course, and recurrence of the inflammatory response, the etiology and pathophysiology of IBD are not completely understood, but mechanism research shows huge potential for clinical applications as therapeutic targets in IBD treatment.
白细胞介素-23(IL-23)是一种促炎细胞因子,主要由抗原刺激后的巨噬细胞和抗原呈递细胞(APCs)产生。IL-23 在介导组织损伤方面发挥着重要作用。事实上,IL-23 及其受体信号的异常与炎症性肠病有关。IL-23 与先天和适应性免疫系统相互作用,IL-23/Th17 似乎参与了慢性肠道炎症的发展。IL-23/Th17 轴可能是这种慢性炎症的关键驱动因素。这篇综述总结了 IL-23 的生物学功能、控制细胞因子产生的细胞因子、IL-23 反应的效应物以及与 IBD 发病机制相关的分子机制的主要方面。尽管 IL-23 调节和影响炎症反应的发展、过程和复发,但 IBD 的病因和病理生理学尚未完全了解,但机制研究表明,作为 IBD 治疗的治疗靶点,具有巨大的临床应用潜力。