The role of Syndecan4 in the development of rheumatoid arthritis

在本研究中，为了了解Syndecan4在类风湿关节炎（RA）发展中的作用，我们在胶原诱导关节炎（CIA）模型中比较了Syn4缺失（Syn4 KO）小鼠和野生型（WT）小鼠。在CIA模型中，Syn4 KO小鼠的临床严重程度和病理特征均有所减轻。Syn4主要在引流LN （dLN）的B细胞上表达，有趣的是，Syn4 KO小鼠在dLN的生发中心形成明显减少。在Syn4 KO小鼠中，参与dLN生发中心形成的B细胞亚群数量也减少。此外，与WT小鼠相比，Syn4 KO小鼠显示出ii型胶原特异性IgG抗体（总IgG， IgG2a和IgG2b）的产生减少。我们的研究结果表明，B细胞上的Syn4可能通过调节生发中心的形成和抗体的产生来调节RA的发生。

In this study, to try to understand the role of Syndecan4 in the development of Rheumatoid Arthritis (RA), we have compared Syn4-deficient (Syn4 KO) mice and wild-type (WT) mice in collagen-induced arthritis (CIA) model. Syn4 KO mice revealed attenuated clinical severity and pathological features in CIA model. Syn4 was mainly expressed on B cells in the draining LN (dLN), and interestingly, Syn4 KO mice showed the drastic hypoplasia of germinal center formation in the dLN. And the numbers of B cell subsets that involve in germinal center formation in the dLN, were also decreased in Syn4 KO mice. In addition, Syn4 KO mice showed reduced production of type-II collagen-specific IgG antibodies (total IgG, IgG2a and IgG2b) compared with WT mice.Our results indicated that Syn4 on B cells possibly regulates the development of RA by modulating germinal center formation and antibody production.