Autoantibodies to gastric mucosa in Helicobacter pylori infection
Although Helicobacter pylori is recognized as the main cause of chronic gastritis and its associated diseases, very little is known about the pathogenetic mechanisms leading to intestinal metaplasia and atrophic gastritis. We reviewed the data regarding the possible pathogenetic role played by the anti-H. pylori immune responses in the genesis of atrophic gastritis and intestinal metaplasia. Although only type A (corpus-restricted atrophic gastritis), often associated to pernicious anemia, is considered autoimmune in nature, abundant evidence supports the presence of cellular and humoral autoimmune responses also in patients with H. pylori infection. In a mechanism known as antigenic mimicry, highly conserved immunogenic molecules expressed by infectious pathogens may act as a trigger for the induction of humoral and cellular immune responses that cross-react with host cellular antigens. Numerous studies support the view that H. pylori is very effective in inducing antigenic mimicry, and antibodies against H. pylori have been found to cross-react with both antral mucosal cells (the membrane of the secretory canalicular structures of the parietal cells) and gastrin-producing cells. Such autoantibodies were detected both in human...Continue Reading
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Autoimmune diseases occur as a result of an attack by the immune system on the body’s own tissues resulting in damage and dysfunction. There are different types of autoimmune diseases, in which there is a complex and unknown interaction between genetics and the environment. Discover the latest research on autoimmune diseases here.
Atrophic Gastritis is a process where gastric glandular cells are lost and replaced with firbous tissues, as a result of chronic inflammation. Learn more about Atrophic Gastritis here.