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Macrophages Steal STING From the Infectious Disease Playbook to Promote Nonalcoholic Fatty Liver Disease.

The stimulator of interferon genes (STING) is a member of a large family of pattern recognition receptors that sense danger signals within cells and activate innate immune responses.1 STING specifically recognizes and responds to nucleic acids present in the cytosol. When activated by nucleic acids, STING triggers a series of events resulting in the production of type I interferons and proinflammatory cytokines2; as such, STING plays a critical role in antimicrobial host defense.3 The classical ligands for STING are double­ stranded DNA molecules from viruses or bacteria. However, STING can also respond to RNA-based microbes and even nucleic acids from host cells.4,5 Its ability to react to “self” nucleic acids has led to an expanded concept of STING as a central figure not only in infectious diseases, but also in the pathogenesis of noninfectious inflammatory diseases.6,7 Recent studies have uncovered a role for STING in diseases affecting the liver. For example, in experimental animals, STING promotes toxic liver injury owing to carbon tetrachloride and ethanol.8,9 In the current issue of Gastroenterology, Luo et al10 extend the liver-related investigation of STING to nonalcoholic fatty liver disease (NAFLD). They report a causal role for STING in murine as well as human NAFLD.