Project/Area Number |
24791144
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
Dermatology
|
Research Institution | University of Yamanashi |
Principal Investigator |
AOKI Rui 山梨大学, 医学部附属病院, 助教 (10377541)
|
Research Collaborator |
KAWAMURA Tatsuyoshi 山梨大学, 医学部附属病院, 講師 (70262657)
SHIMADA Shinji 山梨大学, 医学工学総合研究部, 教授 (10114505)
|
Project Period (FY) |
2012-04-01 – 2014-03-31
|
Project Status |
Completed (Fiscal Year 2013)
|
Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
|
Keywords | マスト細胞 / 単純ヘルペスウイルス / 自然免疫 / HSV |
Research Abstract |
Mast cells are known as important players in innate immune responses. The essential contribution of mast cells to bacterial host defense has been well established; however, little is known about their role in viral infections. We have reported that mast cells were critically involved in host defense at herpes simplex virus 2 (HSV-2)-infected sites through TNF-a and IL-6 production. HSV did not directly induce TNF-a or IL-6 production by mast cells, whereas supernatants from HSV-infected keratinocytes induced production of these cytokines by mast cells. Therefore, we examined which factor derived from HSV-infected keratinocytes activated mast cells. We found that IL-33, known as an alarmin in innate immune responses, was elevated in HSV-infected skin and triggered TNF-a and IL-6 production by mast cells.
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