Fig. 5

Microbial stimulation of inhibitory checkpoints modulates the tumor immune microenvironment. Fusobacterium nucleatum inhibits the activity of natural killer cells and cytotoxic T cells via interaction between Fap2 and TIGIT or CEACAM1. Helicobacter pylori acts on CEACAM1 through its outer membrane protein HopQ protein to inhibit immune cells. Bifidobacterium upregulates the expression of IFN-I in dendritic cells through the STING signaling pathway, thereby promoting antigen cross-presentation and T cell activation to enhance the efficacy of CD47 blockade. Abbreviations: STING = the stimulator of interferon gene