ABSTRACT
Studies of the inflammatory process in the inflamed synovium from rheumatoid arthritis patients have shown an intricate network of molecules involved in its initiation, perpetuation and regulation trial balances the pro- and anti-inflammatory process. This system is self-regulating though the action of anti-inflammatory and pro-inflammatory cytokines cytokine receptor antagonists and naturally occurring antibodies cytokines. Inflammatory synovitis in rheumatoid arthritis (and possibly in other inflammatory arthritidies) appears to be the result of an imbalance in the cytokine network with either an excess production of pro-inflammatory cytokines or from inadequacy of the natural anti-inflammatory mechanisms. Using this knowledge the newer therapeutic approaches to RA and other inflammatory arthritides are being aimed at correcting this imbalance. Monoclonal antibodies to INF-alpha (humanised form of this is called infliximab), soluble TNF-alpha receptors (etanercept) are already in clinical use and adalimumab (humanised TNF-alpha antibody). IL-1Ra is undergoing clinical trials. Other promising therapeutic agents that could regulate the cytokine network are in various stages of laboratory and clinical evaluation. These studies promise to yield therapeutic targets that could dramatically change the way inflammatory diseases would he treated in the future. The now established efficacy of infliximab and etanercept in inflammatory arthritides could be considered just a glimpse of the exciting scenario of the future.