Immunologic aspects of Helicobacter pylori infection and malignant transformation of B cells.

Infection of the human gastric mucosa with Helicobacter pylori induces the development of mucosa-associated lymphoid tissue (MALT), and H pylori-specific local humoral and T-cell responses. H pylori infection also results in the mucosal production of proinflammatory cytokines, which are important in stimulating neutrophil infiltration. Strains of H pylori expressing the cytotoxin associated protein A (CagA) induce gastric epithelial cells to secrete interleukin-8, the neutrophil chemotactic and activating peptide. Variation in the extent of mucosal injury may be a consequence of H pylori strain variability. Gastric B-cell lymphomas of MALT arise from a background of lymphoid follicles, which are acquired in response to H pylori infection. In many cases, eradication of H pylori from patients with low-grade gastric lymphoma results in lymphoma regression, including large tumor masses, implying a causal relationship between H pylori infection and lymphoma growth. Experiments studying the properties of tumor cell and tumor infiltrating T cells in vitro have suggested that rather than stimulating the tumor cells directly, H pylori stimulates tumor infiltrating T cells, which provide help for lymphoma growth. Unlike the active inflammatory response associated with infection with CagA positive strains, but consistent with the acquisition of lymphoid follicles in all infected individuals, the development of MALT lymphomas is independent of bacterial CagA status.