Synovial fibroblasts spread rheumatoid arthritis to unaffected joints.
Synovial fibroblasts spread rheumatoid arthritis to unaffected joints.
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活动性类风湿性关节炎的特点是起源于少数，但随后影响大多数关节。到目前为止，疾病进展的途径在很大程度上是未知的。由于类风湿性关节炎滑膜成纤维细胞（RASFs）是关节破坏和体外迁移的关键参与者，目前的研究评估了RASFs在体内传播疾病的潜力。为了模拟原始关节，将健康人软骨与RASF一起皮下共植入SCID小鼠。在对侧侧腹，植入健康的软骨而不含细胞。RASF显示出通过血管系统向幼稚软骨的主动运动，而不依赖于将RASF应用于SCID小鼠的部位，导致靶软骨的强烈破坏。这些发现支持了以下假设：破坏性关节炎在关节间传播的特征性临床现象至少部分是由激活的RASF的迁移介导的。
Active rheumatoid arthritis is characterized by originating from few but affecting subsequently the majority of joints. Thus far, the pathways of the progression of the disease are largely unknown. As rheumatoid arthritis synovial fibroblasts (RASFs) are key players in joint destruction and migrate in vitro, the current study evaluated the potential of RASFs to spread the disease in vivo. To simulate the primary joint of origin, healthy human cartilage was co-implanted subcutaneously into SCID mice together with RASFs. At the contralateral flank, healthy cartilage was implanted without cells. RASFs showed an active movement to the naïve cartilage via the vasculature independent of the site of application of RASFs into the SCID mouse, leading to a strong destruction of the target cartilage. These findings support the hypothesis that the characteristic clinical phenomenon of destructive arthritis spreading between joints is mediated, at least in part, by the transmigration of activated RASFs.