Fig.3

The impact of gastric microbiota on the modulation of both innate and adaptive immunity within the tumor microenvironment of GC. Innate immunity: Macrophage: Propionibacterium acnes drives the polarization of macrophages into the M2 phenotype by activating TLR4, leading to the secretion of IL-10. pDCs: Stenotrophomonas demonstrates a favorable correlation with the infiltration frequency of pDCs. NK cells: Fusobacterium nucleatum hinders the tumoricidal activity of NK cells by engaging in binding interactions with the inhibitory receptor TIGIT via its Fap2 lectin. ILC2s: H. pylori induces an upregulation in the expression of IL-7R on ILC2s and increases the levels of IL-7 in the gastric environment, thereby promoting the enhanced recruitment of ILC2s. Tumor-activated neutrophils: H. pylori infection induces an elevation in IL-8 secretion, which subsequently attracts the infiltration of neutrophils. F. nucleatum residing in GC cells activates the NF-κB /IL-17 axis, promoting neutrophils recruitment. Adaptive immunity: CD8 + TRM cells: Methobacterium exerts inhibitory effects on TGF-β secretion, leading to a disruption in the residence of CD8 + TRM cells within the gastric epithelium. Effector T cells: H. pylori impedes the recognition of tumor cells by effector T cells by upregulating the expression of PD-L1 within the tumor microenvironment. Treg cells: Selenomonas demonstrates a positive correlation with the frequency of infiltration of Treg cells. H. pylori induces the activation of TLR9 on pDCs, which may contribute to the overexpression of ICOSL and subsequently facilitate the recruitment of Treg cells. Breg cell: H. pylori is associated with the elevation of Breg cells infiltration in the gastric microenvironment