The role of interleukin-32 on inflammatory arthritis and the possibility of being a therapeutic target.
Project/Area Number |
21591959
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Orthopaedic surgery
|
Research Institution | Keio University |
Principal Investigator |
NIKI Yasuo 慶應義塾大学, 医学部, 講師 (10276298)
|
Co-Investigator(Kenkyū-buntansha) |
NAKAYAMA Masanori 慶應義塾大学, 医学部, 助教 (70528249)
KAWASAI Toshiki 慶應義塾大学, 医学部, 助教 (30365291)
|
Project Period (FY) |
2009 – 2011
|
Project Status |
Completed (Fiscal Year 2011)
|
Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2009: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
Keywords | リウマチ病学 / 炎症性サイトカイン / インターロイキン32 / TNF-α / 関節リウマチ / 炎症性関節炎 / Toll様受容体 |
Research Abstract |
IL-32 induces TNF. via NF. B and ERK signaling pathway and contributes to developing inflammatory arthritis through loss of proteoglycan and provocation of synovitis. Since IL-32 induced TNF. had gradually reduced and IL-10 had gradually increased, IL-32 might develop inflammation in early stage and resolve subsequently.
|
Report
(4 results)
Research Products
(11 results)