Gastric autoimmunity: the role of Helicobacter pylori and molecular mimicry.
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.
D'Elios
Mario M
MM
Department of Internal Medicine, University of Florence, 50134 Florence, Italy. delios@unifi.it
Appelmelk
Ben J
BJ
Amedei
Amedeo
A
Bergman
Mathijs P
MP
Del Prete
Gianfranco
G
D000818:Animals; D001324:Autoantigens / Q000276:immunology; D001327:Autoimmune Diseases / Q000201:enzymology / Q000382:microbiology*; D015551:Autoimmunity; D005756:Gastritis / Q000201:enzymology / Q000382:microbiology*; D017506:H(+)-K(+)-Exchanging ATPase / Q000276:immunology*; D016481:Helicobacter Infections / Q000276:immunology; D016480:Helicobacter pylori / Q000276:immunology*; D006801:Humans; D018716:Molecular Mimicry; D010295:Parietal Cells, Gastric / Q000201:enzymology; D018417:Th1 Cells / Q000276:immunology
D001324:Autoantigens; D017506:H(+)-K(+)-Exchanging ATPase