Suppression of B-cell antibody production with human LAG+ Treg and analysis of mechanism of TGF-beta 3

2016 Fiscal Year Final Research Report

• Project/Area Number: 15K19566
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Collagenous pathology/Allergology
• Research Institution: The University of Tokyo
• Principal Investigator: Sumitomo Shuji 東京大学, 医学部附属病院, 助教 (20392996)
• Research Collaborator: TSUCHIDA Yumi ; NAKACHI Shinichiro ; KATO Rika
• Project Period (FY): 2015-04-01 – 2017-03-31
• Keywords: 制御性T細胞 / B細胞 / 抑制性サイトカイン / TGF-β3

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.

Free Research Field

免疫学