Generation of novel inflammatory disease model caused by dysregulation of IL-1 signaling

2014 Fiscal Year Final Research Report

• Project/Area Number: 24500488
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Laboratory animal science
• Research Institution: The University of Tokyo
• Principal Investigator: KAKUTA Shigeru 東京大学, 農学生命科学研究科, 准教授 (80345032)
• Co-Investigator(Kenkyū-buntansha): MATSUMOTO Kiyoshi 信州大学, ヒト環境科学研究支援センター, 教授 (40173893) ; MORI Masayuki 信州大学, 医学(系)研究科(研究院), 准教授 (60273190) ; NAGASE Hisashi 信州大学, 医学部, 助教 (70303451)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 炎症 / 疾患モデル動物 / インターロイキン

Outline of Final Research Achievements

Mice lacking for IL-1 receptor antagonist (Ra), an endogenous inhibitor, spontaneously develop rheumatoid arthritis and psoriasis-like dermatitis. Although it is reported that IL-1Ra consists two isoforms (soluble/s and intracellular/ic) and pre-IL-1α acts as a putative transcriptional factor, their functions remain unknown.
In this study, we newly generated s/icIL-1Ra isoform specific deficient mice and pre-IL1α/NLS mutated mice. Analysis of C57BL/6 background s/icIL-1Ra deficient mice indicates that s/icIL-1Ra isoforms act in a mutually complementary manner. BALB/c background sIL-1Ra deficient mice are novel and useful arthritis model with high breeding efficiency.

Free Research Field

実験動物学