Involvement of gut microbiota in T follicular helper cell-associated immuno senescence
| Project/Area Number |
18K06034
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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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| Review Section |
Basic Section 42040:Laboratory animal science-related
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| Research Institution | Fukushima Medical University |
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Principal Investigator |
Kawata Koji 福島県立医科大学, 医学部, 助教 (20374572)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2020: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 濾胞ヘルパーＴ細胞 / 免疫老化 / 腸内細菌叢 / 老化モデルマウス / 濾胞ヘルパーT細胞 / プロバイオティクス / 老化モデル / SAMP1 |
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| Outline of Final Research Achievements |
In our study, a significant increases of individual T-cell subsets especially T follicular helper (Tfh) cells, which were observed in normal aged mice, were observed in D-galactose-induced aging model mice and senescence accelerated mouse P1 (SAMP1), while antibiotics treatment effectively inhibited the increment of Tfh-like cells. Furthermore, oral administration of Lactobacillus murinus, which was identified as dominant species of intestinal microbiota in antibiotics treated mice, exhibit a similar inhibitory effects. These results suggests that L. murinus might be involved in differentiation and numerical regulation of Tfh-like cells, which might contribute to immunosenescence.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究により、老化に伴うT細胞の構成変化を特定の腸内細菌種によって抑制可能であり、老化病態形成を制御できる可能性が示された。本研究で確認されたTfh様細胞増加の老化病態形成への寄与は明らかとなっていないが、SLEを自然発症するBWF1マウスにおいて、同様の表現型を有するT細胞が若齢期から増加し、病態形成に関与する可能性が報告されている。本研究によって得られた知見は、老化病態のみならず、プロバイオティクス等を用いた自己免疫性疾患コントロールにおいても有用な基礎的データとなると考えられる。
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Report
(4 results)
Research Products
(4 results)
