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The identification of Helicobacter pylori in the pathogenesis of chronic gastritis, peptic ulcer, and gastric cancer has provided an enormous advance in clinical gastroenterology. Epidemiologic studies show that many of the more severe clinical manifestations of H. pylori infection occur in a minority of the infected population. Thus, the interaction among the organism, environmental factors, and the host response contributes to the various forms of disease. This review considers the most recent literature in the context of the hypothesis that gastric diseases associated with H. pylori infection result from a failure in the host's ability to develop an appropriate mucosal immune response to this luminal antigen. A better understanding of the immunopathogenesis of this process will provide a more informed approach for the development of therapeutic intervention through mucosal immunization.