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In mammalian cells, immune responses to viral infection often invoke germ-line–encoded nucleic acid-binding pattern-recognition receptors, the engagement of which results in the induction of type I interferons (IFNs). Following the discovery that intracellular DNA could trigger Toll-like receptor-independent IFN production in a variety of mammalian cells, the relevant signaling pathway was shown to involve TBK1, IRF3, and STING (1⇓⇓–4). However, the major sensor of cytoplasmic DNA remained elusive until the ground-breaking discovery by James Chen and his colleagues of the nucleotidyltransferase cGAS (cGMP-AMP synthase) (5, 6). In this system, recognition of cytoplasmic DNA by cGAS generates a second messenger molecule, cGAMP (cGMP-AMP), which in turn activates the endoplasmic reticulum-resident adaptor protein STING. Activated STING subsequently translocates from the endoplasmic reticulum to the Golgi compartment, where it recruits TBK1 and the transcription factor IRF3, resulting in antiviral gene expression. Because nucleic acids are present in all viruses and are not easily mutated for the “purpose” of recognition-avoidance by a prospective host, innate immune detection of viral nucleic acids appears highly strategic in terms of antiviral defense. However, the use of nucleic acids as pathogen-associated molecular patterns has potential complications, in that self-derived nucleic acids might also pose a risk of triggering …

cGMP-AMP synthase paves the way to autoimmunity