The role of IRF5 in cutaneous inflammation and malignant melanoma
Project/Area Number |
25461685
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Dermatology
|
Research Institution | St. Marianna University School of Medicine (2015) The University of Tokyo (2013-2014) |
Principal Investigator |
Kadono Takafumi 聖マリアンナ医科大学, 医学部, 准教授 (80292910)
|
Project Period (FY) |
2013-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
Keywords | IRF5 / 接触皮膚炎 / 悪性黒色腫 / DNFB / FITC |
Outline of Final Research Achievements |
IRF5 is critical for immunity and induce the production of various inflammatory cytokines to regulate Th1-Th2 balance. In this study, we investigated the role of IRF5 for cutaneous inflammation using contact hypersensitivity model. In IRE5 deficient mice, Th1-type immune responses were significantly reduced, whereas Th2-type immune responses were significantly augmented due to the abnormality in sensitization phase. Dendritic cells are critical for sensitization and inducing immune responses. IRF5-deficient dendritic cells express less IL-12, which presumably leads to reduced Th1-type immune responses. In addition,the number of dendritic cells known to induce Th2-type immune responses were significantly augmented, which might cause increased Th2-type contact hypersensitivity. Thus, IRF5 is critical for balancing Th1-Th2 immune responses.
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Report
(4 results)
Research Products
(2 results)