| ID | 309 |
| Title Transcription | カンセツエン モデル マウス オ モチイタ RANKL シゲキ ジュジョウ サイボウ イニュウ ニヨル メンエキ ヨクセイ キノウ ノ カイセキ
|
| Title Alternative | Immunosuppresive Function of Receptor Activator of NF-кB Ligand (RANKL)-stimulated Dendritic Cells (DCs) for Autoimmune Lesions in Arthritis Models
|
| Author |
Oshima, Jun
Department of Orthodontics, Graduate School of Dentistry, The University of Tokushima
|
| Keywords | 自己免疫疾患
関節リウマチ
樹状細胞
MRL/lprマウス
DBA/1Jマウス
オステオイムノロジー
|
| Content Type |
Departmental Bulletin Paper
|
| Description | 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.
|
| Journal Title |
四国歯学会雑誌
|
| ISSN | 09146091
|
| NCID | AN10050046
|
| Volume | 20
|
| Issue | 1
|
| Start Page | 43
|
| End Page | 59
|
| Sort Key | 43
|
| Published Date | 2007-06
|
| Remark | 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。
|
| FullText File | |
| language |
jpn
|
| Report Type | 学位論文
|
