| Project/Area Number |
15K08917
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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 |
General internal medicine(including psychosomatic medicine)
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| Research Institution | Kobe University |
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Principal Investigator |
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| Research Collaborator |
SHIMIZU Mami 神戸大学, 大学院医学研究科, 医学研究員 (10757313)
INOUE Yuto 神戸大学, 大学院保健学研究科
WAKAFUJI Ryo 神戸大学, 大学院保健学研究科
TAGAMI Kanako 神戸大学, 大学院保健学研究科
NISHIKAWA Minaho 神戸大学, 大学院保健学研究科
SUZUKI Haruka 神戸大学, 大学院保健学研究科
KATSUTA Atsumi 神戸大学, 大学院医学研究科, 研究助手
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | １型糖尿病 / スカべンジャー受容体 / TLR / 病原体感知センサー / 自己免疫 / 1型糖尿病 / スカベンジャー受容体 / NOD / ＴＬＲ / 病原体 / ウイルス / 微生物 |
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| Outline of Final Research Achievements |
Recently, it has been reported that the development of type 1 diabetes would be associated with commensal bacteria. So the aim of this study was to examine the association between scavenger receptor A (SR-A) and Toll-like receptor such as TLR4 on dendritic cells and to establish a new immunological preventative and therapeutic strategy for type 1 diabetes. First, lipopolysaccharide (LPS) as a ligand of TLR4 was administered to female NOD mice and cyclophosphamide (CY) -induced diabetes model in male NOD mice. Second, LPS was administered to SR-A KO NOD mice and CY-induced diabetes model in SR-A KO NOD mice. As a result, LPS administration prevented diabetes onset in all four mouse models. Finally, LPS was administered to 8.3 NOD mice transfected with T cell receptor gene of IGRP-specific CD8 T cell clone into NOD mice, resulting in acceleration of T1D onset. Flow cytometric analysis suggested that the Foxp3 regulatory T cells might play a pivotal role in the mechanism of LPS tolerance.
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