Autophagy and proinflammatory cytokines: Interactions and clinical implications.

•Autophagy is induced by interferon (IFN)-γ, interleukin (IL)-1, tumor necrosis factor (TNF)-α, IL-17, and IL-6, whereas the process is blocked by IL-13, IL-33, IL-10, and IL-4.•Autophagy facilitates the production of IFN-γ, TNF-α, IL-1β and inhibits the secretion of TNF-α, IL-17, IL-1β, IL-α.•Autophagy is a promising target for developing novel therapeutic strategies against inflammatory and infectious diseases.•TNF-α, IL-1β, and IFN-γ promote autophagy and prevent pathogen invasion; Moreover, IFN-γ can promote the generation of immunity in diseases involving immunosuppression.•On the other hand, TNF-α, IL-1β, or IL-17 can trigger excessive autophagy, which contributes to the pathophysiology of several diseases.