Tumour necrosis factor and Crohn's disease.

The production of several pro-inflammatory cytokines is increased in inflammatory bowel diseases (IBD). Experimental models of IBD have further defined the importance of specific cytokines for the induction of mucosal inflammation, by using specific neutralising antibodies, or by silencing cytokine genes in mice by using homologous recombination (knockout mice).' 2 Several therapeutic strategies are now being developed that either target pro-inflammatory cytokines or use recombinant anti-inflammatory cytokines in Crohn's disease and ulcerative colitis. Tumour necrosis factor-a (TNF-a) is a cytokine which can transmit signals between immune and other cells, and is involved in (apoptotic) cell death, metabolism, inflammation, thrombosis, and fibrinolysis. In recent years, an important role for TNF-a as a pivotal pro-inflammatory mediator in Crohn's disease has emerged, and this has resulted in the development of several therapeutic strategies that target TNF-a. This brief review discusses the current status of treatments targeting TNF-a and provides an outlook for future development.