Identification of factors that exacerbate nasal mucosal inflammation associated with ILC2 activation by comprehensive analysis

2019 Fiscal Year Final Research Report

• Project/Area Number: 18K16882
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 56050:Otorhinolaryngology-related
• Research Institution: University of Fukui
• Principal Investigator: Morikawa Taiyo 福井大学, 学術研究院医学系部門, 特別研究員 (70815985)
• Project Period (FY): 2018-04-01 – 2020-03-31
• Keywords: ILC2s / 鼻粘膜肥厚 / M2 マクロファージ

Outline of Final Research Achievements

In this study, we used a mouse model to identify factors that exacerbate nasal mucosal inflammation by group 2 innate lymphoid cells (ILC2s). These factors were significantly elevated in ILC2-induced nasal mucosa of mice, and were significantly suppressed by inhibiting the IL-33/ST2R signaling pathway required for ILC2 activation. These factors were related to M2 macrophages, which were reported to be involved in nasal polyp formation. The results of this study are important for elucidating the mechanism of nasal polyps formation in eosinophilic chronic rhinosinusitis.

Free Research Field

耳鼻咽喉科

Academic Significance and Societal Importance of the Research Achievements

本研究の目的は、好酸球性副鼻腔炎における鼻茸形成、難治性を引き起こすメカニズムを解明することである。最近同定されたアレルギー炎症と関連する新しい細胞集団である2型自然リンパ球(ILC2s)に着目した。本研究では、ILC2による鼻粘膜炎症を関連する因子を同定した。これらの因子が好酸球性副鼻腔炎の病態形成にどのように関与するかを解明することで、指定難病疾患である好酸球性副鼻腔炎の新規治療ターゲットとなる可能性がある。