| Project/Area Number |
16K20438
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pathobiological dentistry/Dental radiology
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| Research Institution | The University of Tokushima |
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Principal Investigator |
SAITO Masako 徳島大学, 大学院医歯薬学研究部(医学域), 助教 (00723892)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | シェーグレン症候群 / 加齢 / 胚中心 / Tfh / 自己免疫疾患 / 自己抗体 / 濾胞性T細胞 |
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| Outline of Final Research Achievements |
We evaluated the mechanism of the formation of autoimmune lesions in SS model mice. The population and cell number of CD4+CD62L-PD-1+ CXCR5+ Tfh cells were significantly higher in SS model mice than in control mice. In addition, the population and cell number of PNA+ GL-7+ CD19+ Germinal center (GC) B cells were significantly enhanced in SS model mice compared with control mice. The areas of expanded GC were significantly increased compared with those of control mice. Furthermore, GC in the spleen of anti-CD20 mAb-treated mice were considerably diminished compared with those of isotype control mAb-treated mice.
These results suggest that anti-CD20 mAb treatment is effective on autoimmune lesions in SS model mice and that B cell depletion suppresses the GC reaction with a reduction of Tfh cells in these mice.
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| Academic Significance and Societal Importance of the Research Achievements |
使用するシェーグレン症候群（SS）モデルマウスは、加齢的に血清自己抗体価の上昇が認められるなど、その病態が、SS患者に極めて類似していることから、このモデルを用いることにより、ヒトSSでは解析が困難であった各種臓 器・組織の病態形成機構に関して、直接的に疾患発症機構について解析を進めることができ、加齢に伴う自己免疫疾患の新たな発症機構を模索できる可能性が極めて高く、その学術的意義は大きい。
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