Helicobacter pylori-derived heat shock protein 60 increases the induction of regulatory T cells (P3365)

Regulatory T cells have been shown to highly infiltrate the H. pylori-infected gastric mucosa. Treg cells suppress the host’s immune responses to H. pylori and dominate during persistent infection. H. pylori-derived HSP60 is one important virulence factor that promotes malignant tumorigenesis. This study further investigated the role of HpHSP60 in immunosuppression, and its activity was found to correlate with the induction of Treg cells. To determine the effects of HpHSP60 on immunosuppression, human peripheral blood mononuclear cells were treated with or without HpHSP60 in the presence of anti-CD3 mAb to determine the effect of HpHSP60 on proliferation. We subsequently asked whether proliferative inhibition correlates with the induction of Treg cells. Finally, the mechanism through which HpHSP60 induces Treg cells was identified. HpHSP60 decreased the expression of CDK4 to significantly slow the proliferation of mitogen-stimulated T cells, which correlated with the induction of Treg cells. Moreover, secretion of IL-10 and TGF-β by monocytic cells was essential to the induction of HpHSP60-induced Treg cells. In summary, we propose that HpHSP60 can act on macrophages to trigger the expression of IL-10 and TGF-β, resulting in an increase in Treg cells and the proliferative inhibition of T cells.