Epithelial and Immune Cell Responses to Helicobacter pylori That Shape the Gastric Tumor Microenvironment

Gastric cancer is the third most common cause of cancer-related death worldwide with a 5-year survival rate of only 29%. The incidence of gastric cancer in the United States is relatively low due to the diagnosis and treatment of the major risk factor Helicobacter pylori (H. pylori). Even after H. pylori infection has been eradicated, there is still a risk of developing gastric cancer. Gastric cancer is the final clinical outcome that is often initiated by a sustained inflammatory response to H. pylori infection and immune cell-epithelial crosstalk. The review focuses on reporting the mechanisms by which the bacterium modulates the host’s innate and adaptive immune response and the gastric epithelium as part of a strategy to create an immunosuppressive microenvironment that ultimately leads to gastric cancer.