Abstract
Autophagy-related (ATG) gene products regulate macroautophagy, LC3-associated phagocytosis (LAP) and LC3-dependent extracellular vesicle loading and secretion (LDELS). These processes also influence antigen processing for presentation on major histocompatibility complex (MHC) molecules to T cells. Here, I summarize how these different pathways use the macroautophagy machinery, contribute to MHC class I and II restricted antigen presentation and influence autoimmunity, tumor immunology and immune control of infectious diseases. Targeting these different pathways should allow the regulation of intracellular and extracellular antigen presentation to T cells to modulate protective and pathological immune responses.
Highlights
Reviewed by: Ludger Klein, Ludwig Maximilian University of Munich, Germany Heung Kyu Lee, Korea Advanced Institute of Science and Technology, South Korea Payel Sil, National Institute of Environmental Health Sciences (NIEHS), United States
The protein kinase complex of ATG1/ULK1 gets inhibited by mammalian target of rapamycin complex 1 and activated by AMP kinase (AMPK) via differential phosphorylation
Proteins with LC3-interacting regions (LIRs) bind to ATG8 orthologues and the phagophore grows around the respective cargo, including damaged mitochondria, chloroplasts, ribosomes, proteasomes, endoplasmic reticulum, protein aggregates, damaged endosomes, bacteria, and some viral capsids
Summary
Autophagy-related (ATG) gene products regulate macroautophagy, LC3-associated phagocytosis (LAP) and LC3-dependent extracellular vesicle loading and secretion (LDELS). These processes influence antigen processing for presentation on major histocompatibility complex (MHC) molecules to T cells. I summarize how these different pathways use the macroautophagy machinery, contribute to MHC class I and II restricted antigen presentation and influence autoimmunity, tumor immunology and immune control of infectious diseases. Targeting these different pathways should allow the regulation of intracellular and extracellular antigen presentation to T cells to modulate protective and pathological immune responses
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