| Project/Area Number |
15K09777
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Dermatology
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
Mineoka Risa 京都府立医科大学, 医学(系)研究科(研究院), 講師 (80464585)
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| Co-Investigator(Kenkyū-buntansha) |
上田 真由美 京都府立医科大学, 医学(系)研究科, 准教授 (60398386)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | アトピー性皮膚炎 / Toll様受容体 / Toll様受容体3 / 自然免疫 / ハプテン / 接触過敏反応 |
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| Outline of Final Research Achievements |
Accumulating evidence suggests that Toll-like receptor (TLR)-3 signaling is involved in non-infectious inflammatory reactions. The exact role of TLR3 in AD remains to be defined. The purpose of this study was to investigate the role of TLR3 in chronic contact hypersensitivity reactions induced by repeated elicitation, resembling the features of AD. Wild-type (WT) and Toll-like receptor 3 knockout (Tlr3 KO) mice were sensitized, and chronic contact hypersensitivity reactions were elicited in their ear skin via repeated application of a hapten, 2,4,6-trinitro-1-chlorobenzene (TNCB) or oxazolone. The Tlr3 KO mice exhibited less ear swelling, less leukocyte infiltration into the skin, and lower serum total IgE levels than WT mice after hapten challenge. The Tlr3 KO mice also displayed lower expression levels of inflammatory cytokines in their TNCB-treated ear skin than WT mice. The results showed that TLR3 deficiency suppressed the development of chronic contact hypersensitivity reactions.
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