Autophagy in inflammation, infection, and immunometabolism

Autophagy is a quality-control, metabolic, and innate immunity process. Normative autophagy affects many cell types, including hematopoietic as well as non-hematopoietic, and promotes health in model organisms and humans. When autophagy is perturbed, this has repercussions on diseases with inflammatory components, including infections, autoimmunity and cancer, metabolic disorders, neurodegeneration, and cardiovascular and liver diseases. As a cytoplasmic degradative pathway, autophagy protects from exogenous hazards, including infection, and from endogenous sources of inflammation, including molecular aggregates and damaged organelles. The focus of this review is on the role of autophagy in inflammation, including type I interferon responses and inflammasome outputs, from molecules to immune cells. A special emphasis is given to the intersections of autophagy with innate immunity, immunometabolism, and functions of organelles such as mitochondria and lysosomes that act as innate immunity and immunometabolic signaling platforms.

Automated summary

Autophagy is a crucial cellular protection mechanism that impacts various diseases when disrupted, including infections, autoimmune diseases, and cancer. It plays a role in clearing harmful substances in and out of cells, protecting against inflammatory damage. The article focuses on the role of autophagy in inflammation, as well as its intersections with immunity, metabolism, and organelle functions.