Chitin-mediated IL-33 induces breakdown of immune tolerance by excessive IL-1b production by DCs, causing aggravation of murine asthma

2016 Fiscal Year Final Research Report

• Project/Area Number: 26461491
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Collagenous pathology/Allergology
• Research Institution: Kyorin University
• Principal Investigator: Arae Ken 杏林大学, 保健学部, 講師 (50306669)
• Co-Investigator(Renkei-kenkyūsha): NAKAE SUSUMU 東京大学, 医科学研究所, 准教授 (60450409) ; MATSUMOTO KENJI 国立研究開発法人国立成育医療研究センター研究所, 免疫アレルギー感染研究部, 部長 (60181765) ; SUDO KATSUKO 東京医科大学, 医学部, 講師 (50126091)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: キチン / Ｔｈ２ / アレルギー

Outline of Final Research Achievements

Chitin, b-(1-4)-poly-N-acetyl-D-glucosamine, is a major constituent of the exoskeleton of house dust mite (HDM), raising the possibility that it may be involved in the development of HDM-related allergic disorders. However, the role of chitin in the pathogenesis of allergic disorders is poorly understood. Chitin enhances Th2-type immune responses in airway such as eosinophilia, IgE production and Th2-cytokine production dependently on the IL-33 production and IL-4/IL-13-STAT-6 pathway, resulting in aggravated OVA-induced airway inflammation in mice. Chitin-mediated IL-33 activates pulmonary DCs to induce excessive IL-1b production, and then the DCs enhance the activation of Th2 cells dependently on antigen and IL-1 signaling.

Free Research Field

免疫学、アレルギー学