2019 Fiscal Year Final Research Report
Exploration of early diagnosis for autoimmune hepatitis by combining lipid metabolism and liver dendritic cells.
| Project/Area Number |
17K08977
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Laboratory medicine
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| Research Institution | Niigata University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
尾関 百合子 新潟大学, 医歯学系, 助教 (00169301)
佐藤 英世 新潟大学, 医歯学系, 教授 (60235380)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Keywords | 自己免疫性肝炎 / 樹状細胞 / 脂質 / 低エストロゲン |
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| Outline of Final Research Achievements |
The purpose of this study was to clarify the relationship between immune tolerance disruption and onset of AIH through lipid metabolism and hepatic dendritic cells. In this study, ovariectomized and high fat diet-fed mice were used as a model of lipid metabolisms disorder. It was suggested that liver injury may be excerbated by a large amount of TNF-α producing hepatic CD11b+ cDCs in OVX mice induced AIH. On the other hand, it was observed that XCR-1+ cDCs accumulate in spleen of high-fat diet mice induced AIH. It was suggested that the mechanism of exacerbation of AIH in high fat diet-fed mice may be different from that in the ovariectomized model.
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| Free Research Field |
免疫学
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| Academic Significance and Societal Importance of the Research Achievements |
自己免疫疾患は免疫寛容の破綻が原因とされているがその発症については未だ解明されていないものが多い。自己免疫性肝炎についても同様であり、近年中年女性だけでなく男性患者の増加や診断時年齢の高齢化の報告もあることから、性差だけではない発症原因が予想される。今回、低エストロゲンモデルと実験的高脂血症モデルを用いて免疫応答を始動する樹状細胞の動態から発症原因を探索することは複雑化している発症原因と免疫寛容破綻との関連性を解明できるため、AIHだけでなく自己免疫性疾患の診断や治療法の基盤作成に貢献できると考えられる。
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