| Project/Area Number |
15K19568
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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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| Research Collaborator |
Teruya Shuzo 東京大学, 医学部附属病院アレルギーリウマチ内科, 大学院生
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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 |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 制御性T細胞 / TGF-beta3 / IL-27 / IL-6 / p28 / Ebi3 |
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| Outline of Final Research Achievements |
LAG3+ Treg, a peripherally-inducible Treg, is reported to show suppressive function through production of TGF-beta3. We have reported that IL-27 can induce TGF-beta3 on mouse naive CD4+ T cell, being endowed with suppressive function. IL-27 consists of p28 and Ebi3, each of which is suggested to have its own function. Interestingly, IL-27+IL-6+p28+Ebi3 combination was the strongest stimuli to induce TGF-beta3 mRNA expression. Moreover, TGF-beta3 mRNA expression was deeply suppressed in p28 or Ebi3 deficient LAG3+ Treg.
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