| Project/Area Number |
26870378
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Collagenous pathology/Allergology
Gastroenterology
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| Research Institution | Shimane University |
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Principal Investigator |
Oshima Naoki 島根大学, 医学部, 助教 (10403461)
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| Research Collaborator |
Yoshikazu Kinoshita 島根大学, 医学部, 教授 (30243306)
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 好酸球性食道炎 / アレルギー / IL-33 / ILC2 / NH細胞 / 自然リンパ球 / 好酸球 |
|---|
| 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.
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