Elucidation of pathogenesis of psoriasis using TRAF3IP/2Act 1 deficient mice and development of new therapy

Research Project

Project/Area Number	25460107
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Multi-year Fund
Section	一般
Research Field	Pharmacology in pharmacy
Research Institution	Nihon Pharmaceutical University
Principal Investigator	Tishio Inoue 日本薬科大学, 薬学部, 准教授 (70458610)
Co-Investigator(Kenkyū-buntansha)	Uramaru Naoto 日本薬科大学, 薬学部, 講師 (90424069)
Project Period (FY)	2013-04-01 – 2016-03-31
Project Status	Completed (Fiscal Year 2015)
Budget Amount *help	¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000) Fiscal Year 2015: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000) Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000) Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Keywords	乾癬 / Traf3ip2/Act1 / JAK/STAT / 掻痒 / 抗ヒスタミン薬 / トファシチニブ / STAT3 / IL-17
Outline of Final Research Achievements	The goal of this study was to explore the mechanisms involved in the pathogenesis of psoriasis using Traf3ip2/Act1 deficient mice. The result suggested that the Traf3ip2/Act1 protein plays an important role in pathogenesis of psoriasis, and were considered can be a new model mice for psoriasis. Moreover, JAK/STAT signaling could be considered as potential therapeutic targets in ameliorating psoriasis.

Report

(4 results)