Unveiling the roles of autophagy in innate and adaptive immunity

By Beth Levine, V. Deretic. Nature reviews. Immunology, 2007

947 citations recorded by the source corpus.

Cells digest portions of their interiors in a process known as autophagy to recycle nutrients, remodel and dispose of unwanted cytoplasmic constituents. This ancient pathway, conserved from yeast to humans, is now emerging as a central player in the immunological control of bacterial, parasitic and viral infections. The process of autophagy may degrade intracellular pathogens, deliver endogenous antigens to MHC-class-II-loading compartments, direct viral nucleic acids to Toll-like receptors and regulate T-cell homeostasis. This Review describes the mechanisms of autophagy and highlights recent advances relevant to the role of autophagy in innate and adaptive immunity.

Subfields: Epidemiology, Parasitology, Public Health, Environmental and Occupational Health

View Paper: https://www.semanticscholar.org/paper/2e69a2aeef91b05d5cc5ea39e3e8d192deca69fd

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Citations in the corpus

Microtubule-associated protein 1 light chain 3 alpha (LC3)-associated phagocytosis is required for the efficient clearance of dead cells (2011, background): “There is a link between autoimmune diseases, such as Crohn’s disease and SLE, and decreased autophagy (40).”
Endoplasmic Reticulum Stress and the Inflammatory Basis of Metabolic Disease (2010, positive): “It is now clear that the autophagy pathway plays an important role in eliminating intracellular pathogens (Levine and Deretic, 2007).”
Absence of autophagy results in reactive oxygen species-dependent amplification of RLR signaling (2009, background): “Recent studies demonstrated that autophagy is used by the cells of the innate and adaptive immune systems to combat viral infections (3, 4).”
Interactions between autophagy receptors and ubiquitin-like proteins form the molecular basis for selective autophagy. (2014, background): “FUNDC1 (FUN14 domain containing 1) is another protein implicated in hypoxia-induced mitophagy (Liu et al., 2012).”
An Overview of the Molecular Mechanism of Autophagy (2009, background): “In addition, autophagy has diverse roles in innate and adaptive immunity (Levine and Deretic 2007).”
Lysosomes as a therapeutic target (2019, background): “of MHCII molecules, T cell homeostasis, antibody pro duction and induction of various immune signals (co stimulation and cytokine secretion) 41 .”
A role for ubiquitin in selective autophagy. (2009, background): “Importantly, coevolution of the pathogens with the host’s innate immune response system has allowed some intracellular bacteria to develop mechanisms that ensure evasion or even hijacking of the autophagic machinery for their own benefit (Levine and Deretic, 2007).”
Autophagy: a lysosomal degradation pathway with a central role in health and disease. (2009, background): “against intracellular pathogens [104,105] by clearing microbes directly via ingestion into autophagosomes for subsequent degradation in”
Defective Hepatic Autophagy in Obesity Promotes ER Stress and Causes Insulin Resistance (2010, background): “Third, there are suggested links between autophagy and immune response (Levine and Deretic, 2007), which exhibit abnormalities in obesity.”
Autophagy in the pathogenesis of disease. (2008, positive): “Recent studies also indicate that autophagy participates in trafficking events that activate innate and adaptive immunity (Levine and Deretic, 2007; Schmid and Munz, 2007).”
Toll‐like receptors control autophagy (2008, background): “Autophagy has a role in innate and adaptive immunity (Levine and Deretic, 2007; Schmid and Munz, 2007) as a”
Plasmacytoid dendritic cells: sensing nucleic acids in viral infection and autoimmune diseases (2008, background): “Recently, autophagy — a conserved cell-autonomous process involving lysosomal degradation of cellular organelle”
Nutrient-dependent mTORC1 association with the ULK1-Atg13-FIP200 complex required for autophagy. (2009, background): “Autophagy is also important for intracellular protein quality control, preimplantation development, degradation of intracellular pathogens, antigen presentation, tumor suppression, and certain types of cell death (Levine and Deretic, 2007; Mizushima et al., 2008; Tsukamoto et al., 2008).”