2016 Fiscal Year Final Research Report
The mechanism of metal allergy construction by a transcription factor controlling immunocompetent cells and a surface reforming effect.
Project/Area Number |
26462851
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Pathobiological dentistry/Dental radiology
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Research Institution | Ehime Prefectural University of Health Science |
Principal Investigator |
TAMAUCHI HIDEKAZU 愛媛県立医療技術大学, 保健科学部, 教授(移行) (60188414)
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Co-Investigator(Renkei-kenkyūsha) |
YAMASHITA KATSUMASA 愛媛大学, 大学院・医学系研究科, 教授 (00311605)
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Project Period (FY) |
2014-04-01 – 2017-03-31
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Keywords | ニッケル / アレルギー / 転写因子 / Th1 / Th2 / NKT細胞 |
Outline of Final Research Achievements |
It suggested that the GATA-3 transcription factor is associated with not only the Th2 type immune response but also the differentiation of NKT cells.The Th2 cells find that they are associated with the sthenia of the response in early period of metal allergy.We made clear that NKT cells functioned for an allergy to metal response restrainingly this time. Also, in the allergy to metal instruction study using the Gfi-1 genetic effect mouse, and determined sthenia of the allergic reaction and determined that pro-an in vitro experiment, an IFN-γ production was enhanced remarkably. Rather than these, it was suggested that the clinical condition of the allergy to metal was built as well as a Th1 type cells in the mechanism of pathogenesis of the allergy to metal by the reciprocal effects of the 2 type cells and NKT cells.
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Free Research Field |
免疫学 アレルギー学
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