Figure 6.

A schematic diagram showing the STING agonist-mediated enhancement of NK cell function. The STING agonist cGAMP promotes the anti-tumor effector functions of NK cells through two pathways. cGAMP directly activates STING signaling in NK cells, leading to the up-regulation of the expression of IFN-β, CD69, CD107a, perforin, granzyme B, and the cytokines IFN-γ, and TNF-α in cGAMP-treated NK cells, which ultimately enhanced the cytotoxicity of NK cells. Alternatively, cGAMP activates STING signaling in pancreatic cancer cells, up-regulates the expressions of NKG2D ligands, and induces the production of chemokines. Thus, cGAMP indirectly activates and recruits NK cells, and enhances the sensitivity of tumor cells to NK cell cytotoxicity.