Generation and Analysis of Antigen-specific T cell-deficient mice by CRISPR/Cas9.

2017 Fiscal Year Final Research Report

• Project/Area Number: 16K14591
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Laboratory animal science
• Research Institution: The University of Tokyo
• Principal Investigator: Watarai Hiroshi 東京大学, 医科学研究所, 特任准教授 (70415339)
• Project Period (FY): 2016-04-01 – 2018-03-31
• Keywords: ゲノム編集

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.

Free Research Field

免疫学