Komatsu Noriko, Takayanagi Hiroshi
Department of Cell Signaling, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo/Global Center of Excellence (GCOE) Program, International Research for Molecular Science in Teeth and Bone Diseases, Japan.
Clin Calcium. 2012 Feb;22(2):179-85.
Rheumatoid arthritis is an inflammation-mediated bone disease characterized by local joint inflammation which results from systemic immune responses. It is essential to clarify the mechanisms by which inflammation elicits bone destruction for the establishment of novel therapeutic strategies. Advances in osteoimmunology, in addition to the development of a various kind of genetically-modified mice and animal models of RA, have greatly contributed to our understanding of these mechanisms. Recently, Th17 cells have been shown to contribute not only to the initiation and amplification of inflammation in RA, but also to bone destruction by enhancing osteoclast differentiation through the interaction with synovial fibroblasts. Thus, Th17-synovial fibroblasts interaction is considered to be a promising therapeutic target for RA.
类风湿性关节炎是一种由炎症介导的骨病，其特征为局部关节炎症，该炎症由全身免疫反应引起。明确炎症引发骨破坏的机制对于制定新的治疗策略至关重要。骨免疫学的进展，以及各种类风湿性关节炎基因改造小鼠和动物模型的开发，极大地促进了我们对这些机制的理解。最近研究表明，Th17细胞不仅在类风湿性关节炎炎症的起始和放大过程中发挥作用，还通过与滑膜成纤维细胞相互作用增强破骨细胞分化，从而导致骨破坏。因此，Th17细胞与滑膜成纤维细胞的相互作用被认为是类风湿性关节炎一个有前景的治疗靶点。
