| Project/Area Number |
25860760
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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 | Osaka Medical College |
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Principal Investigator |
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| Research Collaborator |
HANAFUSA Toshiaki
IMAGAWA Akihisa
HASEDA Fumitaka
FUJISAWA Reiko
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 劇症1型糖尿病 / PD-1 / PD-L1 / PD-L2 / 自己免疫性1型糖尿病 / 全ゲノム解析 / 遺伝子 |
|---|
| Outline of Final Research Achievements |
In this study, we investigated PD-1, which plays an important role in T-cell immune regulation, from genetical and immunological aspects to elucidate the pathogenesis of fulminant type 1 diabetes (FT1D). We found that one polymorphism (7785C/T) in PD-1 gene was associated with autoimmune type 1 diabetes (T1AD), but not with FT1D. PD-1 positivity was significantly lower in CD4+ T-cells in patients with T1AD, but not in those with FT1D. In addition, PD-1 mRNA was significantly lower in CD4+ T-cells in patients with T1AD. These results indicate that low PD-1 expression may be associated with the destruction of beta cells in patients with T1AD via increased T-cell activation.
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