2017 Fiscal Year Final Research Report
Multi-omics analysis of induction mechanism of sjogren syndrome
Project/Area Number |
24689068
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Research Category |
Grant-in-Aid for Young Scientists (A)
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Allocation Type | Partial Multi-year Fund |
Research Field |
Pathobiological dentistry/Dental radiology
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Research Institution | The University of Tokushima |
Principal Investigator |
YAMADA Akiko 徳島大学, 大学院医歯薬学研究部(歯学系), 助教 (70452646)
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Project Period (FY) |
2012-04-01 – 2018-03-31
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Keywords | 自己免疫 / シェーグレン症候群 / 制御性T細胞 / 多層的オミックス解析 |
Outline of Final Research Achievements |
Neonatal thymectomy in certain mouse strains is known to induce autoimmunity due to impaired functions of T cells, including Treg cells. The precise mechanism underlying the induction of autoimmunity by neonatal thymectomy remains unclear. We examined the functions of Treg cells by using a murine Sjogren syndrome model of NFS/sld mice that underwent neonatal thymectomy. The ratio of Treg cells to effector memory phenotype T cells in thymectomy mice was significantly lower than that of nonthymectomy mice. In addition, in vitro induction of peripherally induced Treg cells by TGF-β using naive T cells from Sjogren syndrome model mice was severely impaired. In addition, Treg cells in this Sjogren syndrome model exhibited an interferon-γ producing Th1-like phenotype that resembled effector T cells. In conclusion, these results suggest that abnormal expansion and differentiation of Treg cells and inflammatory cytokines produced by Treg cells contribute to the development of autoimmunity.
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Free Research Field |
免疫学、病理学
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