STING Senses Microbial Viability to Orchestrate Stress-Mediated Autophagy of the Endoplasmic Reticulum.
Inflammasomes detect pathogen-associated molecular patterns to induce inflammatory innate immune responses and play a key role in host defense against infectious agents. However, inflammasomes are often wrongly activated by metabolites, amyloids, and environmental irritants. This induces massive inflammation, causing severe tissue damage, and results in the development of inflammatory diseases. Hence cellular machineries regulating both "activation" and "inactivation" of inflammasomes are definitely important. Recent studies have shown that autophagy, an intracellular degradation system associated with maintenance of cellular homeostasis, plays a key role in inflammasome inactivation. Notably, autophagy deficiency caused by gene mutation disrupts organelle elimination and thus induces aberrant activation of inflammasomes, leading to severe tissue damage. Here we review recent findings regarding the involvement of autophagy in the regulation of inflammasome activation and development of inflammatory disorders.