| Project/Area Number |
24790458
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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 |
Immunology
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| Research Institution | Tohoku University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
MUTA Tatsushi 東北大学, 大学院生命科学研究科, 教授 (60222337)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2012: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 免疫恒常性 / 制御性T細胞 / Foxp3 / IFN-gamma / Treg |
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| Research Abstract |
IkB-family protein, IkB-zeta located into nuclear, and control NF-kB target gene expression. IkB-zeta deficient (KO) mice caused autoimmune like sjogren's syndrome with age.
Thus, we hypothesis that KO mice have problem about the suppressor ability, stability or generation of regulatory T cells (Treg).
We found that regulatory T cells (Tregs) from KO mice has less suppression ability compared with control mice. We also found that stability of Tregs were comparable between control and KO mice. In addition, IkB-zeta plays an pivotal role for Tregs fate desition.
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