[TNF inhibitors: a new therapeutic perspective in chronic inflammatory diseases in rheumatology?]

Interleukin 1 (IL-1) and tumor necrosis factor alpha (TNF alpha) have been identified as important mediators of chronic immuno-inflammatory disease states such as rheumatoid arthritis. Effector cells are triggered by these cytokines to release molecules involved in synovitis and rheumatoid joint destruction, namely prostanoids, leukotrienes, adhesion molecules and metalloproteinases. Modifications of natural inhibitors of IL-1 and TNF alpha, which have been shown to maintain the homeostasis of the cytokine system, are now available by DNA technology. Monoclonal antibodies to TNF and the TNF receptor fusion proteins TNFR 55-IgG and TNFR 75-IgG are currently under clinical investigation in rheumatoid arthritis, inflammatory bowel disease and septic shock. Preliminary results from clinical trials in rheumatoid arthritis suggest that TNF inhibition represents a promising novel interventional strategy providing anti-inflammatory activity and inhibition of effector molecules of structural joint damage.