Helicobacter pylori infection induces accumulation of Vδ1 T cells via CCR2 upregulation

Abstract

SummaryBackgroundWe investigated factors that impact γδ T‐cell phenotype accumulation in Helicobacter pylori‐infected gastric mucosa and peripheral blood.AimTo determine whether H. pylori infection induces accumulation of Vδ1 T cells via CC chemokine receptor 2 (CCR2) upregulation.MethodsMucosal 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, Vδ1 and Vδ2 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 Vδ1 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. Vδ1 T cells were found dominantly residing in H. pylori‐infected gastric mucosa, whereas Vδ2 T cells were mainly found in peripheral blood. Vδ1 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 Vδ1 T cells. Moreover, CCR2 mRNA expression in Vδ1 T cells stimulated with H. pylori components was significantly increased.ConclusionAccumulation of Vδ1 T cells may occur through the upregulation of CCR2 expression.