Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Havard Medical School, Boston, MA 02115, USA.
Immunol Rev. 2010 Jan;233(1):256-66. doi: 10.1111/j.0105-2896.2009.00854.x.
Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease affecting the joint synovium. The normal synovium consists of a lining layer of fibroblast-like synoviocytes (FLS) and macrophages, one to three cells deep that overlies the loose connective tissue of the synovial sublining. During the course of RA, the synovium is the site of inflammation where immune cells are massively infiltrated, and the lining layer becomes hyperplastic and transforms into a pannus tissue that destroys articular cartilage and bone. FLS play an important role in this RA pathogenesis. In this review, we explain that cadherin-11, an adhesion molecule, is selectively expressed on FLS and required for synovial lining formation. In addition, cadherin-11 on FLS contributes to synovial inflammation and mediates cartilage degradation in a mouse model of inflammatory arthritis. Therefore, we suggest that FLS are critical regulators of synovial inflammation and arthritis pathology via mechanisms that are mediated by cadherin-11.
类风湿关节炎（RA）是一种影响关节滑膜的慢性炎症性自身免疫性疾病。正常的滑膜由一层成纤维样滑膜细胞（FLS）和巨噬细胞组成，其覆盖在滑膜下层的疏松结缔组织上，深度为一到三层。在 RA 病程中，滑膜是炎症部位，大量免疫细胞浸润，衬里层增生并转化为血管翳组织，破坏关节软骨和骨。FLS 在这一 RA 发病机制中发挥重要作用。在这篇综述中，我们解释了黏附分子钙黏蛋白 11 选择性地表现在 FLS 上，并需要其形成滑膜衬里。此外，FLS 上的钙黏蛋白 11 有助于滑膜炎症，并在炎症性关节炎的小鼠模型中介导软骨降解。因此，我们认为 FLS 通过钙黏蛋白 11 介导的机制成为滑膜炎症和关节炎病理的关键调节因子。
