Helicobacter pylori infection and gastric autoimmunity: coincidence or cause-effect relationship?

Helicobacter pylori (H. pylori) is a Gram-negative pathogen that causes persistent infection in half the world population. This chapter discusses the possible linkage between H. pylori infection and gastric autoimmunity in humans. It elaborates on the current knowledge of the H. pylori-specific immune response occurring at gastric level in H. pylori-infected patients with different clinical outcomes. The pathogenesis of H. pylori-associated atrophic gastritis associated with the presence of gastric autoantibodies in the serum is also discussed in the chapter. It also reviews and compares the data on classical autoimmune gastritis (AIG)—including recent data on the fine antigen specificity and the functional features of the gastric T-cell response to H+,K+ATPase, the major target autoantigen at the gastric level—with the data obtained in the experimental autoimmune gastritis (EAIG) in animals. The chapter discusses the striking similarities between AIG and H. pylori-gastritis accompanied by corpus atrophy and autoantibodies, together with recent data that allow to reasonably suggest that in some individuals who are genetically predisposed to organ-specific autoimmunity because of their MHC class II haplotype, H. pylori infection plays a role in the induction or exacerbation of gastric autoimmunity through a mechanism of molecular mimicry.