Autophagy is a conserved homeostatic 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 turn, autophagy regulates the production and secretion of a number of cytokines.  In particular, inhibition of autophagy in LPS-treated macrophages and dendritic cells leads to increased secretion of IL-1α, IL-1β, IL-18 and IL-23. The mechanisms underlying these effects differ between cytokines; secretion of IL-1β is dependent on activation of inflammasomes and the TLR2/TLR4 adaptor molecule TRIF, while IL-1α secretion in response to autophagy inhibition is dependent on neither. Moreover, stimulation of autophagy leads to a decrease in intracellular levels of pro-IL-1β, while the secretion of IL-23 in response to inhibition of autophagy is dependent on IL-1. Moreover, supernatants from LPS-stimulated, autophagy-deficient, antigen presenting cells induce the secretion of IL-17, IL-22 and IFN-γ by γδ⁺ T cells, suggesting that autophagy indirectly regulates Th17 responses through the modulation of IL-1 and IL-23. Thus, autophagy represents a potential target for the development of novel therapeutics for the treatment of inflammatory and autoimmune disorders, as well as in the development of treatment strategies for certain infectious diseases and vaccines.