Helicobacter pylori infection induces accumulation of Vδ1 T cells via CCR2 upregulation: HELICOBACTER PYLORI INFECTION CAUSES Vδ1 T-CELL ACCUMULATION

Background We investigated factors that impact gamma delta T-cell phenotype accumulation in Helicobacter pylori-infected gastric mucosa and peripheral blood. Aim To determine whether H. pylori infection induces accumulation of V delta 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 gamma delta, V delta 1 and V delta 2 T cells was evaluated by immunostaining and then compared with counts in 17 patients after H. pylori eradication. TGF-beta, IFN-gamma and CCR2 mRNA expression levels in V delta 1 T cells stimulated by H. pylori component were also evaluated. Results gamma delta 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 delta 1 T cells were found dominantly residing in H. pylori-infected gastric mucosa, whereas V delta 2 T cells were mainly found in peripheral blood. V delta 1 T-cell count was significantly reduced after H. pylori eradication therapy. In in vitro studies, H. pylori component stimulation significantly upregulated both TGF-beta and IFN-gamma production in supernatant from stimulated V delta 1 T cells. Moreover, CCR2 mRNA expression in V delta 1 T cells stimulated with H. pylori components was significantly increased. Conclusion ccumulation of V delta 1 T cells may occur through the upregulation of CCR2 expression.