Exacerbation of endometriosis due to regulatory T cell dysfunction.
| Project/Area Number |
18K16808
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 56040:Obstetrics and gynecology-related
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
Tanaka Yukiko 京都府立医科大学, 医学部附属病院, 専攻医 (50806297)
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| Project Period (FY) |
2018-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2019: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2018: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 子宮内膜症 / 制御性Ｔ細胞 / effector T cell / 子宮内膜症モデルマウス / 炎症性サイトカイン / 制御性T細胞 / 免疫 / Foxp3/DTRマウス / endometriosis / regulatory T cell / cytokine |
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| Outline of Final Research Achievements |
Endometriosis is a chronic inflammatory disorder that is associated with the altered immune response. Regulatory T cells (Treg) play a key role in maintaining immune homeostasis. Here we demonstrate the role of Treg in endometriosis.A mouse model of endometriosis was made by transplanting donor mouse uterine fragments into the abdominal cavity of recipient mice. Foxp3DTR mice were used as Treg cell-depleted model. In Foxp3DTR mice, the number and weight of endometriotic lesions, and the level of inflammatory cytokines and growth factor were significantly increased compared with those in control mice. An enhanced inflammatory response caused by reduced activated Treg cells may be involved in the progression of endometriosis.
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| Academic Significance and Societal Importance of the Research Achievements |
子宮内膜症ではeffector T cellや炎症性サイトカインの増加により免疫応答が生じており、またTregの増加による免疫寛容が子宮内膜の異所性着床を促すのではないかと考えられてきた。この免疫寛容と免疫応答が同時に同部位で生じている矛盾に対しては大きな謎とされてきたが、我々の研究により、子宮内膜症ではTregが減少しており、免疫応答が活性化し、炎症によって子宮内膜症が悪化することが示唆された。これは我々が初めて報告した新たな知見である。
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Report
(3 results)
Research Products
(1 results)
