2012 Fiscal Year Final Research Report
Elucidation of suppressive mechanisms of autoreactive B cells byCD4+CD25-LAG3+ regulatory T cells
| Project/Area Number |
23791106
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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 |
膠原病・アレルギー・感染症内科学
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2012
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| Keywords | 制御性T細胞 / 自己抗体 / 全身性エリテマトーデス / LAG3 / Egr2 |
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| Research Abstract |
The aim of this project is to elucidate the role of Egr2-expressing CD4+CD25-LAG3+ regulatory T cells (LAG3 Treg) in regulation of autoantibody production. Adoptive transfer of LAG3 Treg from control MRL/+ mice to MRL/Faslpr lupus prone mice significantly suppressed the progression of nephritis and autoantibody production. Interestingly, LAG3 Treg co-expressed Egr2 and PD-L1, and LAG3 Treg from T-cell-specific Egr2 conditional knockout or PD1 knockout mice failed to suppress B cell antibody production. These findings elucidate that LAG3 Treg play a crucial role in preventing the excessive B cell responses via Fas/FasL and PD-1/PD-L1 interactions. By exploiting the capacity of LAG3+ Tregs, they may provide a new therapeutic method in autoantibody-mediated autoimmune diseases, including SLE.
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[Journal Article]2012
Author(s)
Izawa S, Okamura T, Matsuzawa K, Ohkura T, Ohkura H, Ishiguro K, Noh JY, Kamijo K, Yoshida A, Shigemasa C, Kato M, Yamamoto K, Taniguchi SI
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Journal Title
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Peer Reviewed
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