Functional analysis of ASK1 in contact hypersensitivity
Project/Area Number |
25860968
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Dermatology
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Research Institution | Tokyo Medical University |
Principal Investigator |
MIZUKAMI Junya 東京医科大学, 医学部, 兼任助教 (30421051)
|
Project Period (FY) |
2013-04-01 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2014)
|
Budget Amount *help |
¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
|
Keywords | ASK1 / IL-17 / contact hypersensitivity / stress response / CHS / MAPK |
Outline of Final Research Achievements |
Contact hypersensitivity is a form of delayed-type hypersensitivity triggered by the response to reactive haptens (sensitization) and subsequent challenge (elicitation). Here, we show that ASK1 promotes CHS and that suppression of ASK1 during the elicitation phase is sufficient to attenuate CHS. The reduced response was concomitant with the strong inhibition of production of IL-17, a cytokine that plays an important role in CHS and other inflammatory diseases, from sensitized lymph node cells. These results suggest that ASK1 is relevant to the overall CHS response during the elicitation phase and that ASK1 may be a promising therapeutic target for allergic contact dermatitis and other IL-17-related inflammatory diseases.
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Report
(3 results)
Research Products
(2 results)
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[Journal Article] ASK1 promotes the contact hypersensitivity response through IL-17 production2014
Author(s)
Mizukami, J. Sato, T., Camps, M., Ji, H., Rueckle, T., Swinnen, D., Tsuboi, R., Takeda, K. and Ichijo, H
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Journal Title
Sci. Rep.
Volume: 4
Issue: 1
Pages: 4714-4714
DOI
NAID
Related Report
Peer Reviewed / Open Access
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