Functional analysis of ASK1 in contact hypersensitivity

2014 Fiscal Year Final Research Report

• Project/Area Number: 25860968
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Dermatology
• 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
• Keywords: ASK1 / IL-17 / contact hypersensitivity / stress response

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.

Free Research Field

皮膚科