Background: Helicobacter (H.) suis is mainly associated with pigs, but is also the most prevalent gastric non-H.pylori Helicobacter species found in humans. Both H.pylori and H.suis may cause persistent infection of the stomach. Several immune evasion mechanisms have been proposed for H.pylori, which focus to a great extent on its major virulence factors, which are absent in H.suis. The aim of this study was to gain more knowledge on immune evasion by H.suis. Materials and Methods: Cytokine expression kinetics were monitored in the stomach of BALB/c mice experimentally infected with H.suis. The cytokine expression profile in the stomach of naturally H.suis-infected pigs was also determined. Subsequently, the effect of H.suis on murine and porcine dendritic cell (DC) maturation and their ability to elicit T-cell effector responses was analyzed. Results: Despite a Th17/Th2 response in the murine stomach, the inflammatory cell influx was unable to clear H.suis infection. H.suis-stimulated murine bone marrow-derived dendritic cells induced IL-17 secretion by CD4(+) cells in vitro. Natural H.suis infection in pigs evoked increased expression levels of IL-17 mRNA in the antrum and IL-10 mRNA in the fundus. In contrast to mice, H.suis-stimulated porcine monocyte-derived dendritic cells were unable to express MHCII molecules on their cell surface. These semimature DCs induced proliferation of T-cells, which showed an increased expression of TGF- and FoxP3 mRNA levels. Conclusions: Helicobacter suis might evade host immune responses by skewing toward a Treg-biased response.