Project/Area Number |
24591635
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Dermatology
|
Research Institution | Keio University |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
YAGUCHI Tomonori 慶應義塾大学, 医学部, 助教 (40424163)
KAWAKAMI Yutaka 慶應義塾大学, 医学部, 教授 (50161287)
|
Research Collaborator |
NAKAMURA Shoko 慶應義塾大学, 医学部, 助教 (20528228)
|
Project Period (FY) |
2012-04-01 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2014)
|
Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
Keywords | 悪性黒色腫 / センチネルリンパ節 / 免疫抑制機構 / TGF-b1 / がん免疫療法 / 免疫抑制 / TGF-β / 免疫病態 / 細胞分子機構 |
Outline of Final Research Achievements |
In cancer patients, sentinel lymph nodes (SLNs) are crucial in the induction of antitumor T cells. However, in many cases, SLNs and tumors appear to be in immune-suppressive condition through mechanisms yet to be elucidated. In this study, the role of tumor-derived TGF-b1 in the generation of immunosuppressive microenvironments of tumors and SLNs was investigated. These results demonstrate that overproduction of TGF-b1 is critical for the generation of immunosuppressive microenvironments in both tumors and SLNs, which may result in suppression of spontaneous antitumor CD8+ T-cell responses. Therefore, TGF-b1 is an attractive target for restoration of immunosuppressive condition in cancer patients.
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