In recent studies a significant association between H. pylori infection and
antigastric autoimmunity has been reported. Antigastric autoantibodies can
be found in more than 30% of infected patients. Two distinct binding patte
rns of these autoantibodies have been described, first at the luminal membr
ane of the foveolar epithelium, and second at the canaliculi membranes of t
he parietal cells in the body mucosa. The latter type of autoantibodies cor
relates with histologic and clinical parameters of gastric mucosa atrophy.
The gastric H,K-ATPase, which is known to be the autoimmune target in class
ical autoimmune gastritis, also represents a major autoantigen in atrophic
H. pylori gastritis. Molecular mimicry between H. pylori and the host does
not seem to be responsible for the generation of this type of autoreactivit
y. The development of antigastric autoantibodies may be a relevant host fac
tor which contributes to the final clinical outcome of chronic H. pylori ga
stritis. (C) 2000 Wiley-Liss, Inc.