| Project/Area Number |
23791036
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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 |
Metabolomics
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| Research Institution | Nagasaki University |
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Principal Investigator |
AKAZAWA Satoru 長崎大学, 大学院・医歯薬学総合研究科, 研究協力員 (50549409)
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| Co-Investigator(Kenkyū-buntansha) |
ABIRU Norio 長崎大学, 大学病院, 講師 (00380981)
KOBAYASHI Masakazu 長崎大学, 大学病院, 助教 (00380874)
KURIYA Genpei 長崎大学, 大学病院, 医員 (50457579)
NAKAMURA Kan 長崎大学, 大学病院, 医員 (70530426)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 1型糖尿病 / T細胞 / IRF / 国際情報交流 |
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| Research Abstract |
To investigate the effectiveness of IRF4 targeting therapy in type 1 diabetes, we generated IRF4 deficient NOD mouse and investigated the phenotypes. We found that progression of autoimmune diabetes / insulitis / autoinsulin antibody were completely suppressed in IRF4-/- NOD mice, also significantly suppressed in heterozygous (IRF4+/-NOD) mice. Adaptive transfer study with combined CD4+and CD8+T cell subsets exhibited that IRF4 is essential for effecter functions in both CD4+ and CD8+ T cells. Less IRF4 expression was associated with reduction of memory T cells and IL-17 producing CD4+T cells, as well as Granzym B producing cells in CD8+T cells. We documented IRF4 is essential for effector function of T cells in autoimmune diabetes in NOD mouse and IRF4 is possible target for prevention for human type 1 diabetes
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