Generation of RORgt+ Innate lymphpid cell deficient mouse

2014 Fiscal Year Final Research Report

• Project/Area Number: 25670228
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Immunology
• Research Institution: The University of Tokyo
• Principal Investigator: SAWA Shinichiro 東京大学, 医学(系)研究科(研究院), 助教 (80611756)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Keywords: 自然リンパ球 / 遺伝子工学 / 腸管免疫

Outline of Final Research Achievements

Group 3 innate lymphoid cell (ILC3) develops RORgt dependent manner and plays critical roles on maintaining mucosal barrier function. In this study, with genetic strategy to dissect T cell and ILC3 development pathway, I generated new mouse model in which ILC3 can be depleted. After double strand DNA break with CRISPR/Cas9 system, loxp franked Diphteria toxin (DTR) transgene was knocked-in to the RORgt locus. I could observe DTR expression on one of the knock-in founders. I am generating ILC3 specifically deletable mice by crossing this KI founders with T cell specific Cre mouse lines.

Free Research Field

免疫学