Researches on regulation of intractable atopic disease by targeting IL-33

2016 Fiscal Year Final Research Report

• Project/Area Number: 26460108
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Pharmacology in pharmacy
• Research Institution: Setsunan University
• Principal Investigator: Nabe Takeshi 摂南大学, 薬学部, 教授 (40228078)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: IL-33 / 喘息 / アトピー / 制御性T細胞 / 抗アレルギー薬

Outline of Final Research Achievements

In the pathogenesis of intractable asthma, IL-33 has been known to be a key molecule bridging between the innate and acquired immune systems. In this study, we analyzed mechanisms underlying IL-33 production, and immunopharmacological modulation of IL-33. Allergic IL-33 production induced by an intratracheal antigen challenge in sensitized mice was mediated by neither mast cells nor Th2 cells. The administered antigen formed an immune complex with the antigen-specific IgG antibody, followed by incorporation into the alveolar macrophages through the cellular suface FcgRII/III, leading to the IL-33 production in the lung. The IL-33 production was sensitive to steroid anti-inflammatory drug treatment. On the other hand, as a new method for regulation of allergy, adoptive transfer of in vitro-differentiated IL-10-producing T cells effectively suppressed asthmatic responses in mice in vivo.

Free Research Field

医歯薬学