Department of Laboratory Medicine, Affiliated Hospital of Jiangnan University, Wuxi, China; Department of Immunology and Infectious Disease, The John Curtin School of Medical Research, The Australian National University, Canberra, Australia.
Arthritis and Tissue Degeneration Program and David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, NY, USA.
Bone. 2022 Nov;164:116540. doi: 10.1016/j.bone.2022.116540. Epub 2022 Aug 27.
Cytokines are an important set of proteins regulating bone homeostasis. In inflammation induced bone resorption, cytokines, such as RANKL, TNF-α, M-CSF, are indispensable for the differentiation and activation of resorption-driving osteoclasts, the process we know as osteoclastogenesis. On the other hand, immune system produces a number of regulatory cytokines, including IL-4, IL-10 and IFNs, and limits excessive activation of osteoclastogenesis and bone loss during inflammation. These unique properties make cytokines powerful targets as rheostat to maintain bone homeostasis and for potential immunotherapies of inflammatory bone diseases. In this review, we summarize recent advances in cytokine-mediated regulation of osteoclastogenesis and provide insights of potential translational impact of bench-side research into clinical treatment of bone disease.
细胞因子是调节骨稳态的一组重要蛋白质。在炎症诱导的骨吸收中,细胞因子(如 RANKL、TNF-α、M-CSF)对于破骨细胞的分化和激活是不可或缺的,这个过程我们称之为破骨细胞生成。另一方面,免疫系统产生许多调节细胞因子,包括 IL-4、IL-10 和 IFNs,限制炎症期间破骨细胞生成和骨丢失的过度激活。这些独特的特性使细胞因子成为维持骨稳态和炎症性骨病潜在免疫治疗的强大靶点。在这篇综述中,我们总结了细胞因子介导的破骨细胞生成调节的最新进展,并提供了将实验室研究转化为临床治疗骨病的潜在转化影响的见解。