Development of therapy for rheumatoid arthritis to correct the dysfunction of dendritic cells caused by human parvovirus B19

在这项研究中，我们的目的是阐明自身免疫的发病机制与细胞因子信号的失调之间的关系，因为我们经历了感染人细小病毒B19的患者，随后发病类风湿关节炎。调节性T细胞（Regulatory T cells, Tregs）是具有抑制免疫功能的主要细胞亚群。然而，Tregs的发展或维持与细胞因子信号传导失调的关系尚不清楚。因此，我们研究了SOCS1在Tregs中的作用，SOCS1是细胞因子- jak - stat通路的负调控。我们明确了SOCS1是Treg功能抑制细胞因子信号传导和Foxp3维持所必需的。

In this study, we have the purpose to clarify the associations between the pathogenesis of autoimmunity and the dysregulation of cytokine signaling, because we experienced patients infected by human parvovirus B19 followed by onset of rheumatoid arthritis. Regulatory T cells (Tregs) are main cell subset to have suppressive immunological functions. However, the development or maintenance of Tregs has not been clarified to be associated with the dysregulation of cytokine signaling. Therefore, we examined the role of SOCS1, which is the negative regulation of the cytokine-JAK-STAT pathway, in Tregs. We clarified SOCS1 is necessary for Treg function to suppress cytokine signaling and Foxp3 maintenance.