About this Research Topic
H. pylori infection of the stomach induces peptic ulcer disease and is a rick factor for the development of gastric cancer. Although over 80% of infected individuals remain asymptomic, all infected subjects develop histologic gastritis. Numerous studies in both mice and humans indicate that the host also develops a regulatory T cell response and that depletion or blocking of these cells results in significantly greater inflammation and T cell recall activity, as well as reductions in bacterial load. The presence and activity of Th1, Th17, and Treg cells in models of H. pylori infection and immunity have been well documented but the mechanisms by which these disparate responses are activated during the course of infection have yet to be elucidated. Therefore, this Research Topic is focuses on the role of the mucosal environment, professional antigen presenting cells, epithelium, and bacterial factors in promoting these T cell responses in the context of both infection and in the induction of protective immunity through vaccination.
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