| Project/Area Number |
16K08749
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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 |
Experimental pathology
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| Research Institution | Baika Women's University (2017-2018)
Kindai University (2016) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
本園 千尋 九州大学, 医学研究院, 助教 (10642910)
宮澤 正顯 近畿大学, 医学部, 教授 (60167757)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | B細胞 / 中和抗体 / レトロウイルス / TLR7 / ウイルス誘発がん / 内在性レトロウイルス / レトロウイルス誘発がん / TLR |
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| Outline of Final Research Achievements |
TLR7 is expressed on several types of cell including dendritic cells and B cells. In this study, we analyzed the requirement of B-cell intrinsic TLR7 for the protection of retrovirus-induced leukemia. Mice lacking of B cell-intrinsic TLR7 produced virus-neutralizing antibodies as efficiently as the wild-type mice by priming of T helper cells, and rapid elimination of exogenous retroviruses were observed. Nevertheless,the B cell-intrinsic TLR7 lacking mice later died of leukemia. These results suggest that B cell-intrinsic TLR7 is essential to regulate the appearance of endogenous and/or recombinant retroviruses even when the virus-specific Th cells are efficiently activated.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究は、B細胞に発現する自然免疫センサーであるウイルス核酸受容体TLR7が、レトロウイルス感染誘発白血病の発症を制御すること、またその白血病発症に内在性レトロウイルスが関与している可能性を示唆した。自然免疫センサーは自己成分の内因性物質にも応答するポテンシャルがあることからも、本研究成果は、ウイルス感染の新たな制御・予防法の開発だけでなく自己免疫疾患等の発症機序を考える上でも有用な情報になると考える。
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