The impact of multidimensional interactions among Helicobacter pylori infection, tumor microenvironment, and gut microbiota on gastric cancer immune response.

Helicobacter pylori (H. pylori) infection is a common bacterial disease of the gastric mucosa, affecting more than 40 % of the global population, and it is classified by the World Health Organization (WHO) as a Group 1 carcinogen for gastric cancer (GC). H. pylori promotes gastric carcinogenesis through complex molecular mechanisms and modulates host immunity via virulence factors (e.g., CagA and VacA), remodeling of the tumor microenvironment (TME), and substantial effects on the gut microbiota-processes that together influence responses to GC immunotherapy. This review synthesizes the multidimensional interplay among H. pylori, host immune responses, and GC immunotherapy across three domains: virulence factors, TME remodeling, and microbiota dysbiosis. We also highlight emerging therapeutic strategies, including nanotechnology-enabled TME reprogramming, stem-cell engineering to derive immune effector cells, and targeted immunomodulation. These approaches offer mechanistic insights and technical platforms for precision immunotherapy in H. pylori-associated GC and may improve prevention and treatment outcomes.