Abstract
Helicobacter pylori (H. pylori) infection and autoimmune inflammation of the gastric mucosa are recognized as the leading etiological factors of chronic atrophic gastritis. The mechanisms of atrophy formation and progression with the risk of gastric cancer development are heterogeneous, which requires a deeper study of the molecular mechanisms of relationship, peculiarities of the course of autoimmune gastritis both in combination with H. pylori and after eradication, as well as without H. pylori infection (naïve AIG). This article presents the specific molecular and cellular patterns in the formation of these related conditions.