| Project/Area Number |
15H05028
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Prosthodontics/ Dental materials science and
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| Research Institution | The University of Tokushima |
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Principal Investigator |
ICHIKAWA Tetsuo 徳島大学, 大学院医歯薬学研究部(歯学系), 教授 (90193432)
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| Co-Investigator(Kenkyū-buntansha) |
渡邉 恵 徳島大学, 病院, 講師 (40380050)
石丸 直澄 徳島大学, 大学院医歯薬学研究部(歯学系), 教授 (60314879)
南 憲一 徳島大学, 病院, 医員 (60732914)
水頭 英樹 徳島大学, 病院, 助教 (70732915)
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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 |
¥16,380,000 (Direct Cost: ¥12,600,000、Indirect Cost: ¥3,780,000)
Fiscal Year 2017: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2016: ¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
Fiscal Year 2015: ¥7,280,000 (Direct Cost: ¥5,600,000、Indirect Cost: ¥1,680,000)
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| Keywords | 歯科用金属アレルギー / 樹状細胞 / 上皮角化細胞 / 金属アレルギー / ケラチノサイト / 金属溶出 |
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| Outline of Final Research Achievements |
The aim of this study is to clarify the mechanisms of sensitization phase of metal allergy development by analyzing the effect of dental metals upon immune cells. We showed dendritic cells (DC) can uptake nickel directly by using fluorescent particles that recognized nickel in vitro and same phenomenon was observed in skin. Expressions of CD100, MAPkinase, and RhoA in DC stimulated with nickel were increased subsequently. This suggested that these cascades might regulate DC’s migration after the uptake of Ni. In addition, expression of plexin B1 and plexin B2 were increased in keratinocytes stimulated with nickel. Therefore, interactions between plexin Bs and CD100 may play an important role in development of sensitization and these interactions have a possibility of using for diagnosis or treatment for metal allergy.
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