摘要：SummaryHelicobacter suis, a zoonotic infection-related bacterium, can induce gastric mucosa-associated lymphoid tissue (MALT) lymphoma in humans and animals. Recently, we reported that the formation of gastric MALT lymphoma afterH. suisinfection is induced by interferon (IFN)-γ activation. Here, we revealed that activation of the Toll-like receptor (TLR) 4–Toll/IL-1 receptor domain-containing adapter-inducing interferon-β (TRIF) pathway afterH. suisinfection is associated with the production of type 1 IFNs (IFN-α, IFN-β) by gastric epithelial cells. Additionally, these type 1 IFNs interact with type 1 IFN receptors on gastric B cells, facilitating the secretion of IFN-γ and the activation of which is enhanced by positive feedback regulation in B cells. These results suggest that the TLR4–TRIF-type 1 IFN–IFN-γ pathway is crucial in the development of gastric MALT lymphoma afterH. suisinfection and may, therefore, represent a therapeutic target for the prevention of this condition.Graphical abstractDisplay OmittedHighlights•H. suisMPLA causes type 1 IFN production in the stomach via TLR4–TRIF signaling•The interaction between type 1 IFNs and IFNAR on B cells causes IFN-γ production•Interaction of IFN-γ and IFNGR on B cells causes IFN-γ positive feedback regulation•IFN-γ from gastric B cells induces gastric lymphoid follicles afterH. suisinfectionBiological sciences; Immunology; Microbiology; Cancer
