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. Author manuscript; available in PMC: 2022 Dec 8.
Published in final edited form as: Vaccine. 2021 Sep 27;39(50):7321–7331. doi: 10.1016/j.vaccine.2021.09.040

Figure 1. Drivers of anti-tumor STING signaling in tumor microenvironment.

Figure 1

Activation of STING/IRF3/TBK1/IFN I in a myeloid cell is achieved (i) endogenously by cGAMP (produced via nucleic acid sensing by cGAS following immunogenic cell death), and exogenously through (ii) recombinant BCG secreting small molecule STING agonist cyclic dinucleotide (CDN) (e.g., c-di-AMP), or (iii) direct administration of CDNs (e.g., c-GAMP). Activated STING activates kinase TBK1 kinase leading to phosphorylation and dimerization of IRF3 which translocate to the nucleus and stimulates the production of Type I IFNs. Type I IFNs act on dendritic cells to promote the induction of tumor-specific T cells and reprogramming of the tumor microenvironment to facilitate anti-tumor responses.