Dynamic Changes of Host Immune Response during Helicobacter pylori-Induced Gastric Carcinogenesis

Abstract

Helicobacter pylori infection is identified as a primary risk factor for gastric cancer (GC). Chronic inflammation is usually induced by H. pylori infection and accompanied by inherent immune disorders. According to Correa’s model, gastritis could progress to premalignant lesions, such as intestinal metaplasia and dysplasia, and ultimately GC. The interaction of H. pylori with the gastric mucosa leads to the recruitment of immune cells, including dendritic (DC) cells, natural killer (NK) cells, and T and B lymphocytes, and triggers inflammatory response with cytokine production, which results in the pathogenesis of stomach. The balance between inflammation and immunity is important to gastric cancer development. However, the dynamic change of immune response during the transition from normal to metaplasia to dysplasia and GC is largely undefined. In this review, we summarized the involvement of key immune cells during GC progression, aiming to help identify inflection points and associated biomarkers for early GC detection, diagnosis, and therapies.