2023 Fiscal Year Final Research Report
Regulation of dental metal allergy symptoms by semaphorins
| Project/Area Number |
21K10003
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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 57050:Prosthodontics-related
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| Research Institution | The University of Tokushima |
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Principal Investigator |
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| Project Period (FY) |
2021-04-01 – 2024-03-31
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| Keywords | 金属アレルギー / ケラチノサイト / セマフォリン |
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| Outline of Final Research Achievements |
In this study, we found that Sema3A expression was upregulated in nickel (Ni)-allergy-induced mouse ear skin tissue and in NiCl2-stimulated mouse keratinocytes. Furthermore, Sema3A regulated TNF-α production and MAP kinase activation in keratinocytes. Specific deletion of Sema3A in keratinocytes by conditional knock out in keratinocytes did not affect the infiltration of immune cells such as dendritic cells and T cells, however attenuated edema and ear swelling. These results indicate that Sema3A potentiates the symptoms of metal allergy and should be explored as a potential target for prevention and treatment of metal allergy.
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| Free Research Field |
歯科補綴学
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| Academic Significance and Societal Importance of the Research Achievements |
金属アレルギーは本質的な病態解明が進んでおらず，発症メカニズムには不明な点が多く残されている．本研究により，金属アレルギーの症状の発現にセマフォリン3Aが関与していることが明らかとなった．アトピー等のアレルギー皮膚炎では，セマフォリン3Aの発現増強が症状の減弱に関与していることが知られており，今回の実験結果と逆の様相を示している．これはセマフォリン3Aが金属アレルギー特有の動きをしており，それ故に金属アレルギー治療のターゲットになる可能性を示している．有効な治療方法を開発する上で，本研究の意義は大きいと考える．
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