Helicobacter pylori causes chronic gastritis in the human stomach, yet only a minority of infected individuals develop peptic ulcer disease, atrophic gastritis, or gastric malignancies. The severity, progression, and consequences of H. pylori infection have been shown to depend on the host genetic background, and in particular on gene polymorphisms affecting the host immune response. Numerous studies published last year brought new information on the mechanisms by which the host genetic make-up modifies the inflammatory and immune responses to H. pylori and the induction of tissue damage secondary to the infection. Novel insights on the regulatory role of H. pylori on the adaptive T-cell response and on its consequences for the persistence of the infection and for the development of vaccines are discussed.