Elucidation of mechanisms underlying IL-23 production from dendritic cells in refractory asthma

2015 Fiscal Year Final Research Report

• Project/Area Number: 25461492
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Collagenous pathology/Allergology
• Research Institution: Chiba University
• Principal Investigator: Tamachi Tomohiro 千葉大学, 医学(系)研究科(研究院), 助教 (20456015)
• Co-Investigator(Kenkyū-buntansha): HIROSE Koichi 千葉大学, 大学院医学研究院, 准教授 (90400887) ; TAKATORI Hiroaki 千葉大学, 医学部附属病院, 助教 (30568225)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 難治性喘息 / IL-23 / 樹状細胞

Outline of Final Research Achievements

To elucidate the underlying mechanisms of refractory asthma, our objective was to identify the factor that induces IL-23 production from dendritic cells. We also aimed to clarify the roles of Dectin-2, a C-type lectin receptor for fungal α-mannan, expressed on dendritic cells and the roles of IκBNS expressed in hematopoietic cells in HDM-induced allergic airway inflammation.
We found Dectin-2 expressed on CD11b+ DCs induced IL-23 expression and promoted HDM-induced airway inflammation. We also found CD11b+ DCs isolated from Dectin-2-deficent mice expressed lower levels of proinflammatory cytokines and co-stimulatory molecules which could lead to Th2 and Th17 cell differentiation than those from wild-type mice. In addition, we found HDM-induced airway inflammation was exacerbated in mice lacking IκBNS in hematopoietic cells. We are currently searching for epithelial cell-derived factors that induce IL-23 production from dendritic cells in asthma by a novel co-culture approach.

Free Research Field

アレルギー学