Tumor necrosis factor (TNF) was originally described as a molecule with antitumor properties released by macrophages stimulated with bacterial products. Almost at the same time that TNF was cloned, it was found to be identical to cachectin, a mediator of cachexia. After the finding of this second aspect of TNF action, several studies demonstrated its role as a proinflammatory cytokine. These studies led to the use of anti-TNF molecules in rheumatoid arthritis and Crohn’s disease. The various strategies used to inhibit TNF are summarized.
