Published online Jun 14, 2017. doi: 10.3748/wjg.v23.i22.3964
Peer-review started: January 21, 2017
First decision: February 9, 2017
Revised: May 16, 2017
Accepted: June 1, 2017
Article in press: June 1, 2017
Published online: June 14, 2017
Processing time: 146 Days and 9.8 Hours
Gram-negative bacteria Helicobacter pylori (H. pylori) colonize gastric mucosa in humans and increase the risk of serious diseases such as gastric and duodenal ulcers, stomach cancers and mucosa associated lymphoid tissue lymphoma. The role of H. pylori infection in the pathogenesis of several extragastric diseases has been suggested including immune thrombocytopenic purpura, iron deficiency anemia, vitamin D deficiency, cardiovascular diseases, diabetes mellitus and dermatological disorders. Also neurological diseases and even lung cancer have attracted researchers concern. The relation between H. pylori infection and a growth retardation in children has also been suggested. Many mechanisms of molecular mimicry between H. pylori and the host have been proposed as a pathogen strategy to manipulate the immune system of the host in order to remain unrecognized and avoid eradication. A lot of effort has been put into the demonstration of homologous sequences between H. pylori and host compounds. However, knowledge about how often autoantibodies or autoreactive T lymphocytes induced during H. pylori infections cause pathological disorders is insufficient. This review provides data on H. pylori antigenic mimicry and possible deleterious effects due to the induction of immune response to the components common to these bacteria and the host.
Core tip: Molecular mimicry between Helicobacter pylori (H. pylori) and the host structures has been suggested as an effective mechanism of antibody production, potentially autoreactive. The chronic character of H. pylori infections increases the risk of such production and initiation or maintenance of H. pylori related pathological disorders triggered by the host effector immune mechanisms during infection. The panel of components common to H. pylori and the host is still increasing and thus the risk of autoimmune complications is an open problem.