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pylori could colonize gastric epithelial cells due to its main components enabling it to survive in an acidic stomach environment and attach to host cells through the interaction of microbial adhesins with host cell receptors through flagellate-mediated motility

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These cells secrete inhibitory cytokines such as TGF- and IL-10, and express immune checkpoint molecules such as PD-L1, jointly weakening the effector functions of cytotoxic CTLs and natural killer cells, thereby promoting tumor immune escape [88]