Involvement of CagA-derived signals, T-cell–derived signals, and tumor microenvironment-related mediators in H pylori–induced lymphomagenesis of gastric MALT lymphoma.H pylori infection stimulates T lymphocytes in the gastric mucosa and indirectly induces the formation of MALT, from which B lymphocytes migrate and infiltrate the site of H pylori infection in the stomach. (A) The CagA protein may be translocated into B lymphocytes as it is secreted by H pylori on gastric epithelial surfaces, thereby resulting in a cascade of survival signaling in the B lymphocytes. (B) H pylori infection can also indirectly promote lymphomagenesis through T-cell–stimulatory pathways such as CD40-mediated signaling and the expression of Th-2–type cytokines and costimulatory molecules such as CD86. H pylori infection can stimulate CD4⁺CD25⁺ Tregs expressing FOXP3. (C) Molecular cross-talk between lymphoma B cells and factors in the tumor microenvironment (T cells and Th17 helper cell-regulated cytokines including IL-22, chemokines, and chemokine receptors) stimulate lymphoma cell survival.