| Project/Area Number |
15K19566
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Collagenous pathology/Allergology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
Sumitomo Shuji 東京大学, 医学部附属病院, 助教 (20392996)
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| Research Collaborator |
TSUCHIDA Yumi
NAKACHI Shinichiro
KATO Rika
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 制御性T細胞 / B細胞 / 抑制性サイトカイン / TGF-β3 |
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| Outline of Final Research Achievements |
LAG3+ Treg identified by the research leaders specifically produces the inhibitory cytokine TGF-β 3 in mice and strongly suppresses antibody production of B cells. In this study, the mechanism of action of TGF-β3 on human primary B cells was elucidated. TGF-β3 inhibited antibody production of human primary B cells, induced cell death of human B cells, inhibited proliferation and inhibited differentiation into plasmablast cells. TGF-β3 suppressed gene expression such as IRF4, Blimp-1, and XBP1, which are important for differentiation into antibody-producing cells, and suppressed phosphorylation of Syk. In addition, in this study, human tonsillar and human peripheral blood LAG3+ Treg were analyzed and the relationship between LAG3+ Treg and rheumatoid arthritis, abatacept was clarified.
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