関節炎モデルマウスを用いたRANKL刺激樹状細胞移入による免疫抑制機能の解析

The pathogenic mechanism of rheumatoid arthritis (RA) is unclear. Many immune cells including T, B cells, and dendritic cells (DCs), or osteoclasts play crucial roles in the development of RA through complex crosstalk between immune and skeletal systems. In this study, the immunoregulatory effect of receptor activator of NF-kB ligand (RANKL)-activated dendritic cells on autoimmune arthritis was analyzed using arthritis models such as MRL/lpr and DBA/1J mice. Three times repeated transfer of RANKL and collagen II-stimulated bone marrow DCs into arthritis models resulted in the regulation of RA via the suppression of T helper function including cell proliferation and Th1 cytokine production. Moreover, the apoptosis of peripheral T cells was increased by the direct interaction of RANKL-activated DCs. These results indicate that activated DCs might play pivotal roles in the pathogenesis of RA through the RANKL-mediated pathway.

公開日:2010年1月24日で登録したコンテンツは、国立情報学研究所において電子化したものです。