Crosstalk between Autophagy and RLR Signaling

Autophagy plays a homeostatic role in regulating cellular metabolism by degrading unwanted intracellular materials and acts as a host defense mechanism by eliminating infecting pathogens, such as viruses. Upon viral infection, host cells often activate retinoic acid-inducible gene I (RIG-I)-like receptor (RLR) signaling to induce the transcription of type I interferons, thus establishing the first line of the innate antiviral response. In recent years, numerous studies have shown that virus-mediated autophagy activation may benefit viral replication through different actions on host cellular processes, including the modulation of RLR-mediated innate immunity. Here, an overview of the functional molecules and regulatory mechanism of the RLR antiviral immune response as well as autophagy is presented. Moreover, a summary of the current knowledge on the biological role of autophagy in regulating RLR antiviral signaling is provided. The molecular mechanisms underlying the crosstalk between autophagy and RLR innate immunity are also discussed.

Automated summary

Autophagy regulates cellular metabolism and acts as a defense mechanism against viral infections. Recent studies have shown that virus-induced autophagy may promote viral replication by modulating host cellular processes, including the regulation of innate immunity mediated by RLR. This article provides an overview of the functional molecules and regulatory mechanisms of RLR antiviral immune response and autophagy, and summarizes the role of autophagy in regulating RLR antiviral signaling and the crosstalk between autophagy and RLR innate immunity.