| Project/Area Number |
25861922
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Surgical dentistry
|
|---|
| Research Institution | University of Toyama |
|---|
Principal Investigator |
TOMIHARA KEI 富山大学, 大学病院, 講師 (70404738)
|
|---|
| Project Period (FY) |
2013-04-01 – 2016-03-31
|
| Project Status |
Completed (Fiscal Year 2015)
|
| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
|
|---|
| Keywords | 口腔癌 / 免疫抑制性細胞 / 抗腫瘍免疫 / マウスモデル / 免疫抑制 / 免疫 / 免疫抑制細胞 |
|---|
| Outline of Final Research Achievements |
In the present study, we conducted immunological study for myeloid derived suppressor cell(MDSC)in a mouse oral cancer model. We investigated whether in vivo administration of chemotherapetuic agent affected the distributions of immune cells, tumor-cell surface expression levels of immune accessory molecules and T cell immune responses in tumor-bearing mice.In vivo administration of chemotherapeutic agent induced significant oral cancer-cell apoptosis in vitro, and chemotherapy markedly attenuated established mouse tumor growth. Chemotherapy decreased the numbers of both myeloid-derived suppressor cells (MDSCs) and B cells in tumor-bearing mice and enhanced dendritic cell maturation. Moreover,chemotherapy upregulated tumor-cell surface expressions of several immune accessory molecules and adhesion molecules, including CD80, CD86, CD40, ICAM-1, VCAM-1, and P-selectin. Remarkably, these tumor cells augmented tumor specific T-cell responses.
|
