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• W1994142348 abstract "Summary Background We investigated factors that impact γδ T‐cell phenotype accumulation in Helicobacter pylori ‐infected gastric mucosa and peripheral blood. Aim To determine whether H. pylori infection induces accumulation of V δ 1 T cells via CC chemokine receptor 2 (CCR2) upregulation. Methods Mucosal biopsy samples from 22 H. pylori‐ free and 75 H. pylori ‐infected patients were classified into grades I–III gastritis groups as per our previous study. The number of γδ , V δ 1 and V δ 2 T cells was evaluated by immunostaining and then compared with counts in 17 patients after H. pylori eradication. TGF‐ β , IFN‐ γ and CCR2 mRNA expression levels in V δ 1 T cells stimulated by H. pylori component were also evaluated. Results γδ T‐cell count was significantly higher in grade III gastritis patients, who exhibited strong IgA and IgG responses to H. pylori urease, than in other groups. V δ 1 T cells were found dominantly residing in H. pylori ‐infected gastric mucosa, whereas V δ 2 T cells were mainly found in peripheral blood. V δ 1 T‐cell count was significantly reduced after H. pylori eradication therapy. In in vitro studies, H. pylori component stimulation significantly upregulated both TGF‐ β and IFN‐ γ production in supernatant from stimulated V δ 1 T cells. Moreover, CCR2 mRNA expression in V δ 1 T cells stimulated with H. pylori components was significantly increased. Conclusion Accumulation of V δ 1 T cells may occur through the upregulation of CCR2 expression." @default.
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• W1994142348 date "2006-12-01" @default.
• W1994142348 modified "2023-09-25" @default.
• W1994142348 title "Helicobacter pylori infection induces accumulation of Vδ1 T cells via CCR2 upregulation" @default.
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• W1994142348 doi "https://doi.org/10.1111/j.1365-2036.2006.00020.x" @default.
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