| Project/Area Number |
24591362
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Endocrinology
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| Research Institution | Osaka University |
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Principal Investigator |
IMAGAWA AKIHISA 大阪大学, 医学(系)研究科(研究院), 准教授 (80373108)
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| Co-Investigator(Renkei-kenkyūsha) |
HANAFUSA Toshiaki 大阪医科大学, 医学部, 教授 (60164886)
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| Research Collaborator |
FUKUI Kenji
NAKATA Shinsuke
YOSHIKAWA Atsushi
HOSOKAWA Yoshiya
BADEN Megu
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 1型糖尿病 / １型糖尿病 / 劇症１型糖尿病 / NK細胞 / KLRC3 / CD94 |
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| Outline of Final Research Achievements |
The aim of the present study was to determine the significance of ISG15, which is induced by viral infection, and KLRC3, which is known as an activating receptor of NK cells in the development of fulminant type 1 diabetes mellitus.
We found that ISG15 acted as an inhibitor of apoptosis by inflammatory cytokines by using overexpression and knockdown methods in MIN6 cells, mouse beta cell line. We also found that the gene expressions of KLRC3 (NKG2E) and CD94, its heterodimer, were reduced in peripheral NK cells of fulminant type 1 diabetic patients.
Overall, we have clarified two candidates of key molecules in the beta cell destruction of fulminant type 1 diabetes.
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