Mechanism of bone and cartilage deterioration in rheumatoid arthritis via RANKL/Fas signaling

在这项研究中，我们研究了人类类风湿关节炎（RA）动物模型MRL/lpr小鼠中携带Fas基因突变的破骨细胞（Ocs）的功能。体外和体内实验表明，MRL/lpr Ocs作为抗原提呈细胞激活外周T细胞的功能增强。此外，MRL/lpr oc对S1P的迁移响应显著增强。MRL/lpr小鼠Ocs功能亢进在RA伴骨破坏的发病机制中起重要作用。细胞的Fas信号可能调控细胞的分化、激活和迁移。

In this study, we investigated the functions of osteoclasts (Ocs) from MRL/lpr mice, animal model for human rheumatoid arthritis (RA), bearinf a mutant of Fas gene. In vitro and in vivo experiments showed enhanced function of MRL/lpr Ocs as antigen-presenting cells to activate peripheral T cells. Furthermore, the migratory response of MRL/lpr Ocs to S1P was significantly enhanced. The hyperfunctions of Ocs in MRL/lpr mice play a potent role in the pathogenesis for RA with bone destruction. Fas signaling of Ocs may regulate the differentiation, activation, and migration of Ocs.