Analysis of molecular mechanism underlying immune disorder during aging
| Project/Area Number |
17K19937
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| Research Category |
Grant-in-Aid for Challenging Research (Exploratory)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Health science and related fields
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| Research Institution | Kansai Medical University |
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Principal Investigator |
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| Research Collaborator |
SUMIYOSHI Mami
KOTANI Yui
WATANABE Toshio
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| Project Period (FY) |
2017-06-30 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥6,500,000 (Direct Cost: ¥5,000,000、Indirect Cost: ¥1,500,000)
Fiscal Year 2018: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
Fiscal Year 2017: ¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
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| Keywords | 胸腺退縮 / mTORC1 / 胸腺上皮細胞 / 免疫老化 / mTEC / cTEC / mTORC1シグナル / 遺伝子改変マウス / 健康年齢 |
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| Outline of Final Research Achievements |
One of the most drastic changes in the immune system during aging is “thymic involution”, which associates with decrease in numbers of thymic T cells as well as thymic epithelial cells. This thymic involution is evolutionally conserved phenomenon in all vertebrates. We have revealed, by using newly developed “artificial” thymic involution system, that mTORC1 signal in the medullary thymic epithelial cells (mTEC) plays an essential role to maintain environment in the thymus. We have already found that loss of mTORC1 signal in mTEC leads to marked decrease in numbers of thymic T cells.
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| Academic Significance and Societal Importance of the Research Achievements |
胸腺退縮の生理的な意義やその分子機構に関しては、適切な老化モデルが少なく、未解明な点が多く残されているのが現状である。本研究により、胸腺上皮細胞のmTORC1シグナルを欠失させることで、人為的に胸腺退縮を引き起こせることが明らかとなった。この系を用いることで、これまで謎に包まれてきた、胸腺退縮の生理的意義解明に繋がることが期待される。
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Report
(3 results)
Research Products
(8 results)
