破骨细胞和白细胞介素-17 在类风湿关节炎发病机制中的作用：关键的“人类破骨细胞学”。
Role of osteoclasts and interleukin-17 in the pathogenesis of rheumatoid arthritis: crucial 'human osteoclastology'.
机构信息
Institute of Rheumatology, Tokyo Women's Medical University, 10-22 Kawada-cho, Shinjuku-ku, Tokyo, 162-0054, Japan.
出版信息
J Bone Miner Metab. 2012 Mar;30(2):125-35. doi: 10.1007/s00774-011-0321-5. Epub 2011 Sep 29.
Many papers have reported that osteoclasts play an important role in the pathogenesis of rheumatoid arthritis (RA); however, when we started to investigate the pathogenesis of RA, the roles of osteoclasts were not highlighted in RA bone resorption. In recent years, the number of articles on the roles of osteoclasts and interleukin (IL)-17 in the pathogenesis of RA has increased exponentially. In this review article, we describe our articles on the roles of osteoclasts and IL-17 in joint destruction in RA, from 1990 to 2011, and highlight a novel term, 'human osteoclastology', which we have used since 2008.
许多文献报道破骨细胞在类风湿关节炎（RA）发病机制中起重要作用；然而，当我们开始研究 RA 的发病机制时，破骨细胞在 RA 骨吸收中的作用并未得到强调。近年来，关于破骨细胞和白细胞介素（IL）-17 在 RA 发病机制中的作用的文章数量呈指数级增长。在这篇综述文章中，我们描述了我们从 1990 年到 2011 年关于破骨细胞和 IL-17 在 RA 关节破坏中的作用的文章，并强调了自 2008 年以来我们使用的一个新术语，“人类破骨细胞学”。
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