Project/Area Number |
25870017
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
General medical chemistry
Experimental pathology
|
Research Institution | Hokkaido University |
Principal Investigator |
Fujikura Daisuke 北海道大学, 人獣共通感染症リサーチセンター, 特任助教 (70547794)
|
Project Period (FY) |
2013-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
Keywords | death receptor 6 / T細胞 / DR6 |
Outline of Final Research Achievements |
Activation of peripheral lymphocytes is a critical step for host protection against infections and tumors. Since ‘high’ activation of the cells induces severe systemic immunological disorders, the activation should be accurately regulated. The regulation depends on the association between several surface molecules that are expressed on the cells. Death receptor 6 (DR6) is an orphan receptor that expresses on peripheral T lymphocytes. However, the detail of the molecule remains unclear. Here, we generated a novel anti-DR6 specific antibody that has an activity for the receptor cross-linking. Using this antibody, we found the induction of DR6 expressing T cells in the disease progression of systemic lupus erythematosus animal model. Administration of the antibody suppressed the activation of T cells. Importantly, the administration also delayed the disease progression of the animal model. These findings indicate that DR6 might be a novel therapeutic target for immunological disorders.
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