Suppression of Th17-inflammation in inflammatory bowel diseases by regulatory T cells
Project/Area Number |
20590743
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Gastroenterology
|
Research Institution | Kyushu University |
Principal Investigator |
NAKAMURA Kazuhiko Kyushu University, 大学病院, 助教 (00274449)
|
Co-Investigator(Kenkyū-buntansha) |
AKIHO Hirotada 九州大学, 大学病院, 講師 (10380411)
MUTA Hiromi 九州大学, 医学研究院, 特別教員 (40325478)
|
Project Period (FY) |
2008 – 2010
|
Project Status |
Completed (Fiscal Year 2010)
|
Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2009: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2008: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
|
Keywords | 下部消化管学(小腸、大腸) / 炎症性腸疾患 / Th17 / 制御性T細胞 |
Research Abstract |
Impaired regulation of immunity in the gut is implicated in the pathogenesis of inflammatory bowel disease (IBD). Regulatory T cells (Treg) possess immnoregulatory activity and are a possible tool for the treatment of IBD. Recent studies suggest that T helper (Th) 1 and Th17 responses are augmented in the gut of IBD. Treg are capable of suppressing Th1-mediated colitis. However, it has not been clarified whether Th17-mediated colitis can be suppressed by Treg. In this study, we demonstrated that Treg are capable of suppressing Th17-mediated colonic inflammation as well as Th1-mediated colitis. It is therefore reasonable to consider utilization of Treg for the IBD treatment even if Th17 is involved in its pathogenesis.
|
Report
(4 results)
Research Products
(9 results)