Antigastric autoimmune reactions in Helicobacter pylori gastritis and their clinical relevance

Recent studies report a significant association between Helicobacter pylori gastritis and autoimmune reaction. Antigastric autoantibodies are detectab le in about 30 % of H. pylori infected patients. Two major in situ binding sites have been found: first, at the luminal membrane of the foveolar epith elium in antrum and corpus mucosa and, second, at canalicular membranes wit hin parietal cells in the corpus mucosa. The presence of latter type of aut oantibodies is correlated with histological and clinical parameters of corp us mucosa atrophy. The gastric H+/K+-ATPase, which is already known as an a utoantigen in classic autoimmune gastritis, also represents a major target in atrophic H. pylori gastritis. According to recent data molecular mimicry between H. pylori and the host does not play a pathogenic role in the form ation these autoantibodies. In conclusion, antigastric autoimmunity represe nts a relevant host factor wh ich contributes to the final outcome of H. py lori gastritis.