Figure 1: Different cytotoxic functions of T cells in H. pylori-related gastric autoimmunity and gastric lymphoma. T cells are essential for defence against infection, but inappropriate Th responses can be harmful for the host. In susceptible individuals, H. pylori induces gastric autoimmunity via molecular mimicry by the expansion of H. pylori-specific T cells that cross-react with epitopes. Cross-reactive T cells would result in destruction of gastric mucosa, by the long-lasting activation of both Fas-ligand (FasL)-induced apoptosis and perforin-mediated cytotoxicity. Conversely, in a minority of infected patients, gastric H. pylori-specific Th cells display deficient cytotoxic control (both perforin and Fas-Fas-ligand mediated) of B-cell growth. Such cytolytic defects, associated with the production of cytokines with B-cell growth factor activity and the chronic delivery of costimulatory signals by Th cells, together with chronic exposure to H. pylori antigens, would result in overgrowth of B cells, thus promoting the neoplastic B-cell transformation and the onset of gastric low-grade MALT B-cell lymphoma.