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Updated: Aug 11, 2025

Author Spotlight: Investigating the Pathophysiology of Eosinophilic Esophagitis
Published on: May 10, 2024
Local type 2 immunity in eosinophilic gastritis.
Netali Ben-Baruch Morgenstern1, Tetsuo Shoda1, Yrina Rochman1
1Division of Allergy and Immunology, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio.
Eosinophilic gastritis (EoG) involves increased T helper 2 (TH2) cells and type 2 cytokines. These TH2 cells correlate strongly with EoG pathology, indicating their role in disease.
Area of Science:
- Immunology
- Gastroenterology
- Cellular Biology
Background:
- Eosinophilic gastritis (EoG) is linked to type 2 immunity.
- The cellular sources of type 2 cytokines and gastric T-cell composition in EoG are not well understood.
- The relationship between gastric T cells and disease pathology requires further investigation.
Purpose of the Study:
- To define gastric T-cell populations in EoG.
- To investigate the association between gastric T cells and EoG pathology.
- To explore the role of T helper 2 (TH2) cells and type 2 cytokines in EoG.
Main Methods:
- Gastric biopsy samples from EoG patients and controls were analyzed using histology, endoscopy, and flow cytometry.
- T-cell populations, including regulatory T cells and TH2 cells, were quantified.
- In a separate cohort, mRNA levels of IL-4, IL-5, and IL-13 were correlated with EoG pathologic parameters.
Main Results:
- Gastric T cells in EoG included increased regulatory T cells and TH2 cells (CD3+CD4+GATA3+) compared to controls.
- TH2 cell levels significantly correlated with gastric eosinophil counts, endoscopic findings, and histopathology.
- Elevated IL-4, IL-5, and IL-13 mRNA levels in EoG also correlated with disease severity.
Conclusions:
- Eosinophilic gastritis is associated with an increase in gastric T helper 2 (TH2) cells.
- These TH2 cells produce type 2 cytokines and their levels strongly correlate with EoG disease pathology.
- The findings highlight the central role of TH2 cells in the pathogenesis of EoG.
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