| Project/Area Number |
18K08304
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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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| Review Section |
Basic Section 53050:Dermatology-related
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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(研究院), 特任准教授 (60398386)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 自然免疫 / IRF3 / 転写因子 / 皮膚 / 接触皮膚炎 / 刺激性皮膚炎 / アトピー性皮膚炎 / Toll様受容体 / 皮膚炎 / アレルギー |
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| Outline of Final Research Achievements |
Interferon regulatory factor 3 (IRF3) is a transcription regulator of cellular responses in many cell types that is known to be important for innate immunity including toll-like receptor 3 (TLR3) signaling. In this study, we examined the role of IRF-3 in allergic and irritant dermatitis by applying a hapten/stimulant singly or repeatedly to the auricular skin of the IRF3-deficient mice. The ear swelling responses in acute/chronic allergic dermatitis and irritant dermatitis were significantly enhanced in the IRF3-deficient mice compared with wild-type mice. In addition, IRF3 deficiency increased leukocyte infiltration into the inflamed skin. Furthermore, the production of some cytokines in the epidermis was increased in the IRF3-deficient mice as compared with wild-type mice. These findings suggest the IRF3 signaling may regulate allergic and non-allergic skin inflammation.
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| Academic Significance and Societal Importance of the Research Achievements |
アトピー性皮膚炎をはじめとするアレルギー性皮膚疾患の病態形成を解明することは非常に重要な課題であるが、その分子機構はいまだに解明されていない点が多い。申請者はこれまでにアレルギー性皮膚炎の病態における自然免疫の役割を解明してきた。本研究で自然免疫のシグナルで重要な役割を果たす転写因子のIRF3の役割が解明されれば、アトピー皮膚炎をはじめとするアレルギー性皮膚疾患の機構についての研究を大きく進展させ、免疫・炎症機構の解明に新たな展開をもたらすことが期待できる。
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