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. Author manuscript; available in PMC: 2019 Apr 1.
Published in final edited form as: Nat Rev Immunol. 2019 Apr;19(4):231–242. doi: 10.1038/s41577-019-0135-6

Fig. 7:|. Activation of the ncDDR in macrophages.

Fig. 7:|

Macrophages activated by signals through Toll-like receptors (TLRs) and interferon receptors produce nitric oxide (NO), which causes genomic DNA double-strand breaks (DSBs) that activate ataxia telangiectasia mutated (ATM) and DNA-dependent protein kinase catalytic subunit (DNA-PKcs), leading to a canonical DNA damage response (cDDR) and a non-canonical DNA damage response (ncDDR). The ncDDR promotes a broadly functional genetic programme in these cells and regulates inflammasome activation. Type I interferon signals are required for optimal cDDR and ncDDR activation. NOS2, nitric oxide synthase.