| Project/Area Number |
20890098
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (Start-up)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
General surgery
|
|---|
| Research Institution | Nagoya University |
|---|
Principal Investigator |
IWASAKI Kenta Nagoya University, 大学院・医学系研究科, 寄附講座助教 (10508881)
|
|---|
| Project Period (FY) |
2008 – 2009
|
| Project Status |
Completed (Fiscal Year 2009)
|
| Budget Amount *help |
¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2009: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2008: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
|
|---|
| Keywords | 移植免疫 / 生体防御 / 補体制御 / シグナル伝達 / 転写 / 転写因子 / 異種移植 |
|---|
| Research Abstract |
It has been observed that a graft organ continues to survive and function normally even in the presence of anti-graft antibodies. However, the mechanisms behind acquirement of this condition remain unknown. Here we report that the anti-HLA ligation on endothelial cells induces PI3K/AKT activation followed by antioxidant gene induction. Activation of PI3K/AKT endothelial cells by a low concentration of anti-HLA ligation enhances protection against complement attack (ref 1 and 2). On the other hands, in ABO-incompatible renal transplantation, we frequently observed C4d deposition on organ without any injury, while C4d binding is related to graft rejection in HLA-incompatible transplantation (not published yet). In future experiment, we will compared signaling events in endothelial cells between anti-ABO and anti-HLA antibody binding and tried to elucidate the mechanisms of accommodation.
|
