Abstract
The aryl hydrocarbon receptor (AhR) is increasingly recognized as a physiologic modulator of the immune response, a function that extends beyond its established role as a sensor for environmental xenobiotics. In a recent report published in the JCI, Cros et al. demonstrate that the AhR restrains tonic, microbiota-driven inflammatory cytokine production in monocytes. Through the combined use of murine models, human ex vivo systems, and the analysis of patient-derived data, Cros and coworkers established that the AhR limits stimulator of IFN gene-induced (STING-induced) proinflammatory signals. These findings define cell type-specific physiologic roles for the AhR in the regulation of innate immunity and underscore its potential as a therapeutic target for the treatment of inflammatory and autoimmune diseases.