徳島大学 教育・研究者情報データベース(EDB)

1. 劉 黎佩(徳島大学大学院口腔科学教育部)

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2. 渡邉 恵([徳島大学.病院.診療科.歯科.そしゃく科(第一補綴科)])

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3. 南 憲一([徳島大学.大学院医歯薬学研究部.歯学域.口腔科学部門.臨床歯学系.口腔外科学])

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4. Yunizar Mohammad([徳島大学.口腔科学研究科.口腔科学専攻])

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5. 市川 哲雄([徳島大学.大学院医歯薬学研究部.歯学域.口腔科学部門.臨床歯学系.口腔顎顔面補綴学])

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(英) Semaphorin 3A: A potential target for prevention and treatment of nickel allergy

(英) Metal allergy is one of the typical immune disorders encountered during the application of dental/medical materials and has a highly complex pathogenic mechanism. Semaphorin 3A (Sema3A), a member of the semaphorin family, is reported to be involved in various immune disorders. However, its role in metal allergy has not been clarified yet. Herein, we show that Sema3A expression was upregulated in nickel (Ni) allergy-induced mouse ear tissue and in NiCl-stimulated mouse keratinocytes. Moreover, Sema3A regulated tumor necrosis factor-alpha production and mitogen-activated protein kinase activation in keratinocytes. The specific deletion of Sema3A in keratinocytes did not affect immune cell infiltration but reduced edema and ear swelling; it also impeded Th1 responses to cause a slight alleviation in Ni allergy in mice. Our results demonstrate that Sema3A promotes the development of metal allergy and should be explored as a potential target for the prevention and treatment of metal allergy.

1. (英) Animals
2. (英) Hypersensitivity
3. (英) Keratinocytes
4. (英) Mice
5. (英) Nickel
6. (英) Semaphorin-3A

1. (英) Article.ELocationID: 10.1038/s42003-022-03641-0

2. (英) Article.PublicationTypeList.PublicationType: Journal Article

3. (英) Article.PublicationTypeList.PublicationType: Research Support, Non-U.S. Gov't