Essential role of interleuikin-33-induced innate lymphoid cells in development of eosinophilic esophagitis in mice

2017 Fiscal Year Final Research Report

• Project/Area Number: 26870378
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Collagenous pathology/Allergology; Gastroenterology
• Research Institution: Shimane University
• Principal Investigator: Oshima Naoki 島根大学, 医学部, 助教 (10403461)
• Research Collaborator: Yoshikazu Kinoshita 島根大学, 医学部, 教授 (30243306)
• Project Period (FY): 2014-04-01 – 2018-03-31
• Keywords: 好酸球性食道炎 / アレルギー / IL-33 / ILC2

Outline of Final Research Achievements

Eosinophilic esophagitis (EoE) is a chronic inflammatory disorder of the esophagus characterized by mucosal infiltration of eosinophils. Interleukin (IL)-33 is a member of the IL-1 cytokine family that is constitutively expressed in epithelial cells. Epithelial-derived IL-33 induces innate lymphoid cell group 2 (ILC2) activities in various organs, which subsequently activates Th2 cytokines and leads to development of eosinophil-related allergic diseases. However, little is known regarding the roles of IL-33 and ILC2 activity induced by it in the pathogenesis of EoE. In the present study, several experimental protocols were designed to clarify these issues.　 Our results clearly show that IL-33-induced ILC2 cell activity leads to infiltration of esophageal mucosa by eosinophils via production of Th2- and allergy-related cytokines, which may play an important role in EoE development.

Free Research Field

消化器内科学