The current model of gastric carcinogenesis comprises the interaction of multiple risk factors. Besides Helicobacter pylori (H. pylori) infection as the major risk factor for gastric carcinogenesis, environmental factors (e.g. high saline- or nitrosamine-containing food) and genetic susceptibility contribute to the development of gastric cancer (GC). It has been established that the topographical pattern of gastritis and its immune response are the main causes for the persistence of bacteria and the final clinical outcome. Regulatory immune cells, mostly regulatory FOXP3(+)CD4(+)CD25(+high) T-cells (Treg cells), have been identified as the major regulatory component of the adaptive immune response and involved in H. pylori-related inflammation and bacterial persistence. The functional activity of these cells is either mediated by direct cell-cell contact or by the secretion of the immune-modulating cytokines TGF-beta1 and IL-10. Based on the differentiation process, Treg cells comprise various lineages that differ in the expression of cell surface marker and pattern of secreted cytokines. Numerous studies have demonstrated important functions of Treg cells for controlling acute and chronic inflammatory processes. This paper reviews the role of Treg for gastric carcinogenesis and precursor lesions related to H. pylori.