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FOXP3+ regulatory T cells in children with Helicobacter pylori Infection
- FOXP3+ regulatory T cells in children with Helicobacter pylori Infection
- Cho K.Y.Y.; Cho M.S.; Seo J.W.
- Ewha Authors
- 서정완; 조민선
- SCOPUS Author ID
- 서정완; 조민선
- Issue Date
- Journal Title
- Pediatric and Developmental Pathology
- Pediatric and Developmental Pathology vol. 15, no. 2, pp. 118 - 126
- SCI; SCIE; SCOPUS
- Document Type
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- Despite an intensive pro-inflammatory response, the immune system is unable to clear the organism in Helicobacter pylori gastritis. Regulatory T (Treg) cells, which suppress the immune response of antigen-specific T cells, have recently been demonstrated to play a key role in chronic inflammation by immunologic tolerance. The purpose of our study was to investigate the histopathology, FOXP3+CD4+CD25highTreg (FOXP3+ Treg) cell expression, and immune responses in children with H. pylori infection. Twenty-four H. pylori-positive and 24 H. pylori-negative children who underwent esophagogastroduodenoscopy for dyspeptic symptoms were included. Histopathologic grading according to the updated Sydney classification and immunohistochemical stains for FOXP3, transforming growth factor- β1 (TGF-β1), and CD4 were performed. Histopathologic bacterial density score, gastritis activity score, and chronic inflammation score were higher in the H. pylori-positive group than in the negative group (P < 0.01). The number of FOXP3+Treg cells and CD4 +T cells and the grade of TGF-β1 expression were significantly increased in the H. pylori-positive group compared to the negative group (P < 0.01). The number of FOXP3+Treg cells correlated positively with the grade of TGF-β1 expression regardless of H. pylori status (P < 0.05). The number of FOXP3+Treg cells and the grade of TGF-β1 expression correlated positively with H. pylori density, gastritis activity score, and chronic inflammation score regardless of H. pylori status (P < 0.01). These findings indicate that FOXP3+Treg cells could play a role in persistent H. pylori infection. © 2012 Society for Pediatric Pathology.
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