Department of Rheumatology, Erasmus MC, University Medical Center, Rotterdam, The Netherlands.
Department of Immunology, Erasmus MC, University Medical Center, Rotterdam, The Netherlands.
Eur J Immunol. 2018 Feb;48(2):220-229. doi: 10.1002/eji.201646787. Epub 2018 Jan 15.
The IL-23/Th17 axis has been implicated in the development of autoimmune diseases, such as rheumatoid arthritis (RA) and psoriatic arthritis (PsA). RA and PsA are heterogeneous diseases with substantial burden on patients. Increasing evidence suggests that the IL-23 signaling pathway may be involved in the development of autoimmunity and erosive joint damage. IL-23 can act either directly or indirectly on bone forming osteoblasts as well as on bone resorbing osteoclasts. As IL-23 regulates the activity of cells of the bone, it is conceivable that in addition to inflammation-mediated joint erosion, IL-23 may play a role in physiological bone remodeling. In this review, we focus on the role of IL-23 in autoimmune arthritis in patients and murine models, and provide an overview of IL-23 producing and responding cells in autoimmune arthritic joints. In addition, we discuss the role of IL-23 on bone forming osteoblasts and bone resorbing osteoclasts regarding inflammation-mediated joint damage and bone remodeling. At last, we briefly discuss the clinical implications of targeting this pathway for joint damage and systemic bone loss in autoimmune arthritis.
IL-23/Th17 轴被认为与自身免疫性疾病的发展有关，如类风湿关节炎 (RA) 和银屑病关节炎 (PsA)。RA 和 PsA 是异质性疾病，给患者带来了巨大的负担。越来越多的证据表明，IL-23 信号通路可能参与自身免疫和侵蚀性关节损伤的发生。IL-23 可以直接或间接地作用于成骨细胞和破骨细胞，从而调节骨形成和骨吸收。由于 IL-23 调节骨细胞的活性，因此可以想象，除了炎症介导的关节侵蚀外，IL-23 可能在生理骨重塑中发挥作用。在这篇综述中，我们重点关注 IL-23 在自身免疫性关节炎患者和小鼠模型中的作用，并概述自身免疫性关节炎关节中产生和应答 IL-23 的细胞。此外，我们还讨论了 IL-23 对炎症介导的关节损伤和骨重塑过程中成骨细胞和破骨细胞的作用。最后，我们简要讨论了针对该通路治疗自身免疫性关节炎关节损伤和全身骨质流失的临床意义。
