Elucidation of the role of IL-23 in bronchial asthma caused by skin barrier dysfunction and drug discovery application

2016 Fiscal Year Final Research Report

• Project/Area Number: 26461198
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Respiratory organ internal medicine
• Research Institution: Keio University
• Principal Investigator: Kagawa Shizuko 慶應義塾大学, 医学部(信濃町), 研究員 (80645507)
• Co-Investigator(Renkei-kenkyūsha): Fukunaga Koichi 慶應義塾大学, 医学部, 専任講師 (60327517) ; Suzuki Yusuke 慶應義塾大学, 医学部, 特任講師 (80306696) ; Kubo Akiharu 慶應義塾大学, 医学部, 専任講師 (70335256)
• Research Collaborator: Kabata Hiroki ; Masaki Katsunori ; Mochimaru Takao ; Matsusaka Masako
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 経皮感作 / 皮膚バリア / IL-23

Outline of Final Research Achievements

Th17 cells are the main cells that produce IL-17A.We found that IL-23 is required for the differentiation of Th17 cells via a patch application on the skin.In oder to find a therapeutic target of percutaneous sensitized asthma, I focused on the role of IL-23 produced in the local skin region and the role of Th17 in cytokine enhancement by administrating anti-IL-23 or control IgG to a percutaneously sensitized asthma mouse model, and then evaluating it for eosinophilic airway inflammation In the group to which the anti-IL-23 antibody was administered during the sensitization phase, the production of OVA-specific IgG1 antibody tended to decrease compared to the group to which the control IgG antibody was administered, and furthermore, the bronchoalveolar lavage fluid eosinophil count and eosinophil infiltration in tissues were found to decrease significantly.

Free Research Field

皮膚科学