Numerous cytokines are present within inflammatory foci. Interleukin-1 (IL-1) and tumour necrosis factor (TNF) play a major role in coordinating mechanisms which command inflammation. Upon their action, many different cells produce lipidic mediators, proteolytic enzymes, and free radicals, all directly responsible for the noxious effects observed. IL-1 and TNF exert cytotoxic effects on vascular endothelium, cartilage, bone and muscle. Such cytokines as interferon-gamma, IL-3 or granulocyte-macrophage colony stimulating factor amplify the inflammatory response by increasing the production of IL-1 and TNF. The latest trigger the release of chemokines such as IL-8 and macrophage chemoattractant protein-1, the chemotactic activity of which participates in the recruitment of leukocytes within the foci of inflammation. IL-6, abounds in inflammatory processes and induces the production by hepatocytes of acute phase proteins. The same applies to IL-1, TNF, IL-11, the leucocyte inhibitory factor, and the transforming growth factor-beta. The later also processes a number of anti-inflammatory activities and, like IL-4, IL-10 and IL-13, can inhibit IL-1 and TNF production. Such property has also been mentioned for interferon-alpha. These anti-inflammatory cytokines can also counteract some of the IL-1 and TNF activities such as those reported during the coagulation process. Furthermore, these anti-inflammatory cytokines can induce the production of the IL-1 receptor antagonist which prevents the activities initiated by IL-1. Soluble TNF receptors, released during inflammation, are the direct inhibitors for TNF. Glucocorticoids, produced following a cascade of events initiated by IL-1, TNF and IL-6, involving the neuroendocrine axis, also inhibit proinflammatory cytokine productions. The concept of "cytokine network" therefore, perfectly illustrates the participation of these mediators in inflammation mechanisms.