Studies indicate that, among a number of other cytokines, interferons (IFN alpha, beta and gamma) are important elements regulating acute as well as chronic inflammatory responses. The role of interferons has been investigated in various experimental models of inflammation, by administration both of interferons and of antibodies that block the biological activity of interferons formed endogenously. The conclusions reached from these experiments clearly indicate that interferons can boost as well as inhibit inflammation. The effects depend on the type of inflammation studied, the time of interferon administration or emergence in the tissue, the type of interferon (alpha/beta or gamma), the dosage, and the presence of other inflammation-controlling cytokines. The effect of blockage of IFN gamma by the systemic administration of neutralising antibodies is particularly clear. Such blockage has been found to profoundly modify local lipopolysaccharide (LPS)-induced inflammation, brain inflammation due to autoimmunity or infection, and shock reactions caused by systemic administration of LPS. Further research on the particular place occupied by interferons in the inflammation-controlling cytokine network holds great promise, not only for better understanding but also for improved therapy of acute and chronic inflammatory disease.