The role of Syndecan4 in the development of rheumatoid arthritis

为了了解Syndecan4在类风湿性关节炎(RA)发病中的作用，我们在胶原诱导性关节炎(CIA)模型中比较了Syn4缺陷(Syn4 KO)小鼠和野生型(WT)小鼠。Syn4KO小鼠在CIA模型中表现出临床严重程度和病理特征的减轻。Syn4主要表达在引流性LN(DLN)的B细胞上，有趣的是，Syn4 KO小鼠在DLN中表现出生发中心形成的严重发育不良。Syn4KO小鼠DLN中参与生发中心形成的B细胞亚群数量也减少。此外，与WT小鼠相比，Syn4KO小鼠产生的II型胶原特异性抗体(总IgG、IgG2a和IgG2b)减少。我们的结果表明，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.