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. 2022 Dec 23;24(1):245. doi: 10.3390/ijms24010245

Figure 3.

Figure 3

DNA damage promotes immune response. Endogenous or exogenous genotoxic stress triggers the accumulation of DNA damage, thereby forming DNA fragments. The DNA sensor cGAS binds to the DNA and uses GTP and ATP to catalyze the synthesis of cGAMP. cGAMP activates the endoplasmic reticulum (ER)-bound STING. NF-κB released from IkBa is activated and translocates into the nucleus, where it induces transcriptional targets, including cytokines. The secreted IFNs binds to their heterodimeric receptor IFNAR1/2 or IFNGR1/2 and activates JAK phosphorylation of STAT1 and STAT2. The STAT1/2 heterodimer acts as a transcription factor and triggers the expression of cytokines (such as IL18, IL15, CCL20). STAT1/2 heterodimer acts as a transcription factor and triggers the expression of cytokines such as IL18, IL15, and CCL20.Cytokines activate immune effector cells (i.e., natural killer cells and T cells) by promoting tumor antigen/neoantigen presentation on the major histocompatibility complex I (MHC-I) and PD-1/ PD-L1 expression.