| Project/Area Number |
13671238
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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 |
General surgery
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| Research Institution | The University of Tokushima |
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Principal Investigator |
KURITA Nobuhiro (2002) The University of Tokushima, University Hospital, Assistant, 医学部附属病院, 助手 (30335814)
松村 敏信 (2001) 徳島大学, 医学部・附属病院, 講師 (00263814)
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| Co-Investigator(Kenkyū-buntansha) |
ITAKURA Mituo The University of Tokushima, Institute for Genome Research, Professor, ゲノム機能研究センター, 教授 (60134227)
栗田 信浩 徳島大学, 医学部・附属病院, 助手 (30335814)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2002: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2001: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Keywords | NOD mice / Autoimmnity / Islet transplantation / Diabetes / サイクロフォスファミド / サイクロフォスファシド / TGF-β1 / I型糖尿病 |
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| Research Abstract |
We produced NOD-RGP-TGF-β1 mice in which pTGF-β1 is expressed in islet ac cells of NOD mice under the control of the rat glucagon promoter. Islets of NOD-RGP-TGF-β1 mice were transplanted to spontaneously diabetic NOD mice. The all grafts of NOD-RCP TGF-β1 mice in spontaneously diabetic NOD mice was rejected within 10 days post-transplantation. The diabetogenic dose of CY (200mg/kg) was additionally injected two times to NOD-RGP-TGF-β1 mice or littermates after islet transplantation. All littermates were induced hyperglycemia by single injection of CY. However, none of NOD-RGP-TGF-β1 mice were induced hyperglycemia by single injection of CY and three out of four NOD-RGP-TGF-β1 mice remained normoglycemia by second injection of CY. As a result, the protection mechanism against autoimmune diabetes in NOD mice by local paracrine TGF-β1 is not direct protction against effector lymphocytes, but decrease of generation of autoreactive T cells and the generation of regulatory T cells
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