Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany.
Front Immunol. 2019 Jul 3;10:1483. doi: 10.3389/fimmu.2019.01483. eCollection 2019.
Rheumatoid arthritis (RA) is a chronic inflammatory disease, characterized by autoimmunity that triggers joint inflammation and tissue destruction. Traditional concepts of RA pathogenesis have strongly been focused on inflammation. However, more recent evidence suggests that autoimmunity modulates the disease and in particular bone destruction during the course of RA. RA-associated bone loss is caused by increased osteoclast differentiation and activity leading to rapid bone resorption. Autoimmunity in RA is based on autoantibodies such as rheumatoid factor (RF) and autoantibodies against citrullinated proteins (ACPA). These autoantibodies exert effector functions on immune cells and on bone resorbing osteoclasts, thereby facilitating bone loss. This review summarizes potential pathways involved in increased destruction of bone tissue in RA, particularly focusing on the direct and indirect actions of autoantibodies on osteoclast generation and function.
类风湿关节炎（RA）是一种慢性炎症性疾病，其特征为自身免疫触发关节炎症和组织破坏。RA 发病机制的传统概念主要集中在炎症上。然而，最近的证据表明，自身免疫调节疾病，特别是在 RA 病程中调节骨破坏。RA 相关的骨丢失是由破骨细胞分化和活性增加导致的快速骨吸收引起的。RA 中的自身免疫基于类风湿因子（RF）和针对瓜氨酸化蛋白的自身抗体等自身抗体。这些自身抗体对免疫细胞和破骨细胞发挥效应功能，从而促进骨丢失。本文综述了 RA 中骨组织破坏增加的潜在途径，特别是重点关注自身抗体对破骨细胞生成和功能的直接和间接作用。
