| Project/Area Number |
16K07082
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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 animal science
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| Research Institution | Chiba University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
有馬 雅史 獨協医科大学, 医学部, 准教授 (00202763)
幡野 雅彦 千葉大学, 大学院医学研究院, 教授 (20208523)
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| Project Period (FY) |
2016-10-21 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2018: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 免疫応答 / 疾患モデル |
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| Outline of Final Research Achievements |
In order to elucidate the role of the double-stranded RNA editing enzyme ADAR1 (adenosine deaminase acting on RNA-1) in adaptive immunity, we have analyzed mice deficient in ADAR1 specifically for activated T cells or B cells. In both activated T-cell and B-cell-specific ADAR1-deficient mice, differentiation of Germinal Center (GC) -Tfh cells and GC-B cells after immunization with NP-CG / Alum or OVA / Alum was suppressed, and high affinity IgG antibody and OVA-specific IgE antibody were significantly reduced. These results indicate that ADAR1 plays an extremely important role in the adaptive immune system by acting endogenously on T cells and B cells and by being involved in T-B cell interactions.
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| Academic Significance and Societal Importance of the Research Achievements |
免疫後のリンパ球の機能分化や機能制御における詳細なメカニズムは未だ明らかでない。我々は獲得免疫にける機能が明らかでないADAR1について注目し、本研究により特にGC-Tfh細胞やGC-B細胞の機能にADAR１が重要な役割を果たすことを見出した。本研究の成果は、今後、GC-Tfh細胞とGC－B細胞の分化や機能の制御機構の研究および免疫システムの解明研究において意義があると考えられる。また本研究の成果はアレルギー性疾患やHIVなど有効なワクチンが存在しない感染症に対する効果的なワクチン療法の開発へとつながる点に社会的に意義がある。
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