Helicobacter pylori induces in-vivo expansion of human regulatory T cells through stimulating interleukin-1β production by dendritic cells

Helicobacter pylori is one of the most common infections in the world. Despite inciting inflammation, immunological clearance of the pathogen is often incomplete. CD4(+)CD25(hi)forkhead box protein 3 (FoxP3(+)) regulatory T cells (T-regs) are potent suppressors of different types of immune responses and have been implicated in limiting inflammatory responses to H.pylori. Investigating the influence of H.pylori on T-reg function and proliferation, we found that H.pylori-stimulated dendritic cells (DCs) induced proliferation in T-regs and impaired their suppressive capability. This effect was mediated by interleukin (IL)-1 beta produced by H.pylori-stimulated DCs. These data correlated with in-vivo observations in which H.pylori(+) gastric mucosa contained more T-regs in active cell division than uninfected stomachs. Inciting local proliferation of T-regs and inhibiting their suppressive function may represent a mechanism for the chronic gastritis and carcinogenesis attributable to H.pylori.