| Project/Area Number |
22590432
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Immunology
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| Research Institution | Yamagata University |
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Principal Investigator |
|
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| Co-Investigator(Kenkyū-buntansha) |
NARA Hidetoshi 山形大学, 医学部, 助教 (00375338)
|
|---|
| Co-Investigator(Renkei-kenkyūsha) |
ASAO Naoki 東北大学, 理学系研究科, 教授 (60241519)
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| Project Period (FY) |
2010 – 2012
|
| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | サイトカイン / IL-21 / Ape1/Ref-1 / 炎症性腸炎 / TH17 |
|---|
| Research Abstract |
We found that IL-21 induced Ape1/Ref-1 protein and that the redox regulatory activity of Ape1/Ref-1 was essential for IL-21-induced ERK1/2 activation. To investigate the functional role of Ape1/Ref-1 in T cell differentiation and activation, we treated CD4^+ T cell with Ape1/Ref-1 redox inhibitor. The inhibitor upregulated IFN-. production from CD4^+ T cell, therefore Ape1/Ref-1 might control TH1/TH17 balance. We are now researching that the inhibitor can modulate DSS-induced colitis in IL-21isoform transgenic mice, which show more severe phenotype of colitis with TH17 cell accumulation than the wild type mice.
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