2021 Fiscal Year Final Research Report
Novel mechanism of endometrial ovarian cyst related to sterile inflammation
Project/Area Number |
19K09813
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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 |
Review Section |
Basic Section 56040:Obstetrics and gynecology-related
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Research Institution | Nippon Medical School |
Principal Investigator |
Ikeda Mariko 日本医科大学, 医学部, 助教 (10740988)
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Co-Investigator(Kenkyū-buntansha) |
明樂 重夫 日本医科大学, 医学部, 教授 (40231849)
根岸 靖幸 日本医科大学, 医学部, 准教授 (50644580)
桑原 慶充 日本医科大学, 医学部, 准教授 (40373013)
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Project Period (FY) |
2019-04-01 – 2022-03-31
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Keywords | 子宮内膜症 / 自然免疫 / 獲得免疫 / HMGB1 / アラーミン / 炎症 |
Outline of Final Research Achievements |
This study aimed to investigate the involvement of high-mobility group box-1 (HMGB1) in an inflammatory milieu and the characteristics of immune cells in endometrial ovarian cyst (EOC). The cytoplasmic HMGB1 levels in dendritic cells (DCs), macrophages, and non-immune cells were analyzed by flow cytometry. We also evaluated the proportions of immune, T, NK, iNKT, NK, and regulatory T (Treg) cells. Results showed that the DCs, macrophages, and non-immune cells of EOC had significantly higher cytoplasmic HMGB1 levels than those of non-EOC (nEOC). The expression of CD69 and CD107a on CD8+ T and CD4+ T cells of EOC was also more enhanced than that of nEOC. Furthermore, the M2 macrophages and Tregs highly accumulated in EOC. These results indicate that HMGB1 may aggravate chronic inflammation related to T-cell activation and simultaneously facilitate development of the immunosuppressive milieu in EOCs.
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Free Research Field |
子宮内膜症
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Academic Significance and Societal Importance of the Research Achievements |
月経困難症、過多月経、性交痛、不妊症など女性のライフクオリティを著しく損なう疾患である子宮内膜症の未解明な病態について、免疫学的アプローチを行うことによりその発症や増悪因子の可能性を見出すことが出来た。今後、治療方針の究明などに繋げていくことが出来れば、子宮内膜症に悩む多くの女性患者の生活の改善に寄与することが出来ると考えている。また子宮内膜症を患う女性の年代は多くが30-40代である。職種を問わず、これらの年代の女性のライフクォリティが上昇することは、社会の活性化に繋がる可能性も秘めていると思われる。
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