| Project/Area Number |
25860803
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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 |
IWASAKI Yukiko 東京大学, 医学部附属病院, 助教 (30592935)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | IL-27 / 制御性T細胞 / Egr2 / 制御性Ｔ細胞 / 全身性エリテマトーデス / LAG3 |
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| Outline of Final Research Achievements |
We have recently reported the CD4+CD25-LAG3+ new regulatory T cells (LAG3 Treg), which specifically express the transcriptional factor early response gene 2 (Egr2). The applicant has already found that interleukin (IL)-27 cytokine can induce both Egr2 and LAG3 on naive CD4-positive T cells. In this project, it was shown that the IL-27-induced CD4-positive T cells can suppress antibody production from B cells. In addition, the applicant revealed that IL-27 signal can be transduced by the transcriptional factor signal transducer and activator of transcription 3 (STAT3), resulting in Egr2 expression. These findings provide insights into the novel therapeutic potential for systemic lupus erythematosus (SLE).
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