| Project/Area Number |
26640054
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Laboratory animal science
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| Research Institution | Shiga University of Medical Science |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
NAKAMURA Shinichiro 滋賀医科大学, 動物生命科学研究センター, 准教授 (50307980)
ITOH Yasushi 滋賀医科大学, 医学部, 准教授 (90324566)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 子宮内膜症 / カニクイザル / LAP陽性細胞 / 免疫抑制細胞除去カラム / Treg / 内膜症サル / LAP陽性単球 / NK細胞 / 体外循環 / 免疫抑制 |
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| Outline of Final Research Achievements |
Cynomolgus macaques with endometriosis decreased NK activity, suggesting that they would not have eradicated endometrial tissues spilled into the peritoneum. In the ectopic endometrial tissues, Treg increased and M2 macrophages significantly increased.
In two macaques, extracorporeal circulation with a column absorbing immunosuppressing cells could decrease lesion of ectopic endometrial tissues. After the treatment, analysis of peripheral blood showed decrease of latency associated protein (LAP)-positive monocytes. All together, it seemed that Treg and LAP positive monocytes with potential to M2 macrophages were critical for pathogenesis of endometriosis.
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