[Helicobacter pylori infections and autoimmunity: the interplay in the pathogenesis of gastritis]

Recent studies suggest a significant association of Helicobacter pylori (H.p.) gastritis and antigastric autoimmunity. Sera of H.p. infected patients exhibit antigastric autoantibodies with high prevalence (over 50 percent of the cases) and with antiluminal and/or anticanalicular binding patterns on gastric mucosa. Models for the pathogenesis of this H.p. associated autoimmunity are antigenic mimicry or Th 1-induced expression of MHC class II and costimulatory molecules on gastric epithelial cells. The anticanalicular autoantibodies binding to gastric parietal cells show fine specificities for the alpha- and for the beta-subunit of the gastric H, K-ATPase, which correspond to the findings in classical autoimmune gastritis. They are significantly correlated with higher grades of corpus gastritis as well as morphologic and functional glandular atrophy of the corpus. The development of this antigastric autoimmunity apparently is a relevant pathogenic factor of the host reaction and might be crucial for the different types and outcomes of H.p. gastritis.