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Host specific T-cell response is critical for the outcome of Helicobacter pylori infection. In genetically susceptible individuals, H. pylori can activate gastric CD4+ Th1 cells that recognize cross-reactive epitopes shared by H. pylori proteins and self H+, K+-ATPase, leading to gastric autoimmunity via molecular mimicry.

The gastric mucosal pathogen Helicobacter pylori induces autoantibodies directed against the gastric proton pump H + ,K + -ATPase in 20–30% of infected patients. The presence of these autoantibodies is associated with severity of gastritis, increased atrophy, and apoptosis in the corpus mucosa, and patients with these autoantibodies infected with H. pylori display histopathological and clinical features that are similar to those of autoimmune gastritis (AIG). This review will focus on the T helper cell responses, cytokines, and adhesion molecules involved in corpus mucosal atrophy in chronic H. pylori gastritis and in AIG, and the role of H. pylori in the onset of AIG. [ABSTRACT FROM AUTHOR]

Human autoimmune gastritis (AIG) is a chronic inflammatory disorder of the gastric corpus. We have defined the antigen repertoire and the functional properties of in vivo activated CD4 + T cells derived from the gastric mucosa of patients with AIG. A remarkable proportion of the CD4 + T cell clones proliferated in response to H + ,K + -ATPase. Six epitopes identified in the α chain, and 5 in the β chain, of gastric K + ,K + -ATPase were recognized by autoreactive gastric T cell clones. The majority of the autoreactive T cell clones secreted IFN-γ and showed a T helper 1 (Th1) profile. All clones produced TNF-α,provided help for B cell immunoglobulin production, expressed perforin-mediated cytotoxicity, and most induced Fas-Fas ligand-mediated apoptosis. Data suggest that activation of gastric H + ,K + -ATPase-specific Th1 T cells is crucial in the pathogenesis of human gastric autoimmunity and atrophy. [ABSTRACT FROM AUTHOR]