Vertebrate immune systems must be able to process and respond to myriad intrakingdom and interkingdom interactions by commensals and pathogens. Counterintuitively, Lima-Junior et al. found that colonization of mouse skin by the bacterium Staphylococcus epidermidis initiates an antiviral immune program. Sensing of S. epidermis by keratinocytes induced the expression of endogenous retroviruses that could be detected by the host’s cGAS–STING signaling pathway. This pathway promotes the tissue repair function of commensal-specific T cells. Antiretroviral treatment impairs repair processes, whereas a high-fat diet enhances endogenous retrovirus expression, leading to excess skin inflammation. Thus, the immune system integrates the endogenous virome and exogenous microbiome into a fruitful alliance.
Cell 184, P3794 (2021).
