Suppressive effect of IL-27 on corticosteroid-resistant severe asthma

2021 Fiscal Year Final Research Report

• Project/Area Number: 20K17224
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 53030:Respiratory medicine-related
• Research Institution: Keio University
• Principal Investigator: MOCHIMARU Takao 慶應義塾大学, 医学部(信濃町), 共同研究員 (60594570)
• Project Period (FY): 2020-04-01 – 2022-03-31
• Keywords: 2型自然リンパ球 / IL-27 / Toll-like receptor 7

Outline of Final Research Achievements

Group 2 innate lymphoid cells (ILC2s) induce corticosteroid-resistant eosinophilic inflammation and are associated with the pathophysiology of severe asthma. We previously found that IL-27 is a potent suppressive cytokine for ILC2s. In this study, we found that Toll-like receptor 7(TLR7) agonist stimulates interstitial macrophages to produce IL-27 in the lung, which contribute to suppression of ILC2-mediated airway inflammation

Free Research Field

免疫アレルギー

Academic Significance and Societal Importance of the Research Achievements

ILC2はステロイド抵抗性を獲得する故、その制御方法は不明な点が多い。今回IL-27がヒト由来のILC2に対して有力な抑制サイトカインであることを明らかにし、さらに生体内でIL-27を効率よく誘導しILC2を抑制する方法を見出した。この知見がILC2を介した喘息病態に対する新たな治療につながる可能性が期待される。