Gastric autoimmunity: the role of Helicobacter pylori and molecular mimicry

Trends Mol Med. 2004 Jul;10(7):316-23. doi: 10.1016/j.molmed.2004.06.001.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Autoantigens / immunology
  • Autoimmune Diseases / enzymology
  • Autoimmune Diseases / microbiology*
  • Autoimmunity
  • Gastritis / enzymology
  • Gastritis / microbiology*
  • H(+)-K(+)-Exchanging ATPase / immunology*
  • Helicobacter Infections / immunology
  • Helicobacter pylori / immunology*
  • Humans
  • Molecular Mimicry*
  • Parietal Cells, Gastric / enzymology
  • Th1 Cells / immunology


  • Autoantigens
  • H(+)-K(+)-Exchanging ATPase