Gastric autoimmunity: the role of Helicobacter pylori and molecular mimicry

Abstract

Pathogens can induce autoreactive T cells to initiate autoimmune disease by several mechanisms. Pathogen-induced inflammation results in the enhanced presentation of self antigens, which causes the expansion of the activated autoreactive T cells that are required for disease onset. Alternatively, a pathogen might express antigens with epitopes that are structurally similar to epitopes of autoantigens, resulting in a mechanism of molecular mimicry. This is the case for Helicobacter pylori-associated human autoimmune gastritis, in which the activated CD4+ Th1 cells that infiltrate the gastric mucosa cross-recognize the epitopes of self gastric parietal cell H(+)K(+)-ATPase and of various H. pylori proteins. Therefore, in genetically susceptible individuals, H. pylori infection can start or worsen gastric autoimmunity, leading to atrophic gastritis.