A novel molecule that regulates T-cell tolerance under PD-1.
Project/Area Number |
21790465
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Single-year Grants |
Research Field |
Immunology
|
Research Institution | Kyoto University |
Principal Investigator |
CHIKUMA Shunsuke Kyoto University, 医学研究科, 助教 (50437208)
|
Project Period (FY) |
2009 – 2010
|
Project Status |
Completed (Fiscal Year 2010)
|
Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2009: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
Keywords | 免疫寛容 / 自己免疫 / 免疫抑制受容体 / 免疫学 / 自己免疫疾患 / がん免疫 / 免疫制御 |
Research Abstract |
ITAG-1 was first identified as a novel molecule that was uniquely suppressed by PD-1 mediated inhibitory signal in T-cells. Analyses using newly generated ITAG-1 knockout mice revealed ITAG-1's role in the terminal development of cytotoxic T-cells. Although, the precise mechanism is still under investigation, current data suggested PD-1 mediated modulation of ITAG-1 expression is involved in T cell activation, differentiation and tolerance.
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Report
(3 results)
Research Products
(8 results)