| Project/Area Number |
16K14591
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Laboratory animal science
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| Research Institution | The University of Tokyo |
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Principal Investigator |
Watarai Hiroshi 東京大学, 医科学研究所, 特任准教授 (70415339)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | ゲノム編集 / CRISPR/Cas9 / iNKT細胞 / 肥満 / CD1d / ゲノム |
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| Outline of Final Research Achievements |
Here we have successfully generated new Traj18－/－ mouse lines by using the Clustered Regularly Interspaced Short Palindromic Repeat (CRISPR)/Cas9 technology. The CRISPR-Traj18－/－ mice lacked iNKT cells and harbored an undisturbed TCRα repertoire, fulfilling the criteria of iNKT cell-deficient mice.
Divergent findings for the metabolic role of iNKT cells have been reported in studies using the previously generated Traj18－/－ mouse strain. Therefore, we re-investigated the contribution of iNKT cells to the development of obesity induced by a high-fat diet (HFD) using our novel Traj18－/－ mouse strain on the B6 background.Among the experimental groups on HFD, CRISPR-Traj18－/－ (1-1L) mice gained less weight than WT B6 mice. The CRISPR-Traj18－/－ mouse strain on HFD also exhibited ameliorated metabolic phenotypes, which is consistent with a pathogenic role of iNKT cells in the development of obesity and insulin-resistance.
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