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

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 Vδ1 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, 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.

Conclusion

Accumulation of Vδ1 T cells may occur through the upregulation of CCR2 expression.