title: Autophagy and cytokines.
abstract: Autophagy is a highly conserved homoeostatic mechanism for the lysosomal degradation of cytosolic constituents, including long-lived macromolecules, organelles and intracellular pathogens. Autophagosomes are formed in response to a number of environmental stimuli, including amino acid deprivation, but also by both host- and pathogen-derived molecules, including toll-like receptor ligands and cytokines. In particular, IFN-γ, TNF-α, IL-1, IL-2, IL-6 and TGF-β have been shown to induce autophagy, while IL-4, IL-10 and IL-13 are inhibitory. Moreover, autophagy can itself regulate the production and secretion of cytokines, including IL-1, IL-18, TNF-α, and Type I IFN. This review discusses the potentially pivotal roles of autophagy in the regulation of inflammation and the coordination of innate and adaptive immune responses.
authors: Immunology Research Centre, School of Biochemistry & Immunology, Trinity College Dublin, College Green, Dublin 2, Ireland. jaharris@tcd.ie
authors: James
authors: J
authors: Harris
mesh_terms: D001343:Autophagy / Q000502:physiology*; D016207:Cytokines / Q000502:physiology*; D006801:Humans; D008024:Ligands; D051193:Toll-Like Receptors / Q000378:metabolism
chemical_list: D016207:Cytokines; D008024:Ligands; D051193:Toll-Like Receptors