Inflammation as an Etiologic Agent of Gastric Cancer.

. We and others have shown that atrophy can also be induced by the secreted immune products (cytokines) of a type I/Th1 or Th17 immune response. The atrophic phase of gastritis is superseded by a metaplastic, or cellular redifferentiation phase driven by type II (Th2) cytokines. The outcome of this inflammatory sequela is dysplasia of the gastric epithelium; the substrate for multiple types of gastric cancers. Here we summarize our recent findings on Th1/Th17 and Th2 immune responses and their roles in driving gastric atrophy, metaplasia, and carcinogenesis. Importantly, these cytokines and their receptors represent promising therapeutic targets for the prevention and treatment of gastric cancer.