| Project/Area Number |
15H06374
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Collagenous pathology/Allergology
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| Research Institution | Osaka University |
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Principal Investigator |
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| Project Period (FY) |
2015-08-28 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 全身性エリテマトーデス / 自己免疫疾患 / T細胞受容体 / 制御性T細胞 / 抗CD3抗体 / T cell receptor / antibody responses / regulatory T cells / ①Ｔ細胞受容体 / ②抗体産生反応 / ③自己免疫疾患 / 抗体 / 自己免疫 |
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| Outline of Final Research Achievements |
For quantitative down-modulation of T-cell receptor, we used anti-CD3 F(ab')2 antibody. In vivo injection of the antibody resulted in the temporal reduction of TCR intensity (around 20% vs controls) by flow cytometric analysis. When wild-type mice were immunized with NP-CGG, formation of germinal center B cells were significantly reduced, however, follicular helper T cell number were comparable in antibody-treated group. Notably, we found that the number of regulatory T cells (Tregs) were significantly increased by F(ab')2 antibody treatment. To address whether the reduction of antibody responses is due to direct inhibition of Tfh induction or through the induction of Treg, we will use Treg depletion models and/or Treg transfer models using Foxp3-DTR mice and/or Foxp3-GFP mice.
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