COMMENTARY

Inflammatory bowel disease

Life and death in the gut: more killing, less Crohn's

A Sturm, C Fiocchi

Division of Gastroenterology, University Hospitals of Cleveland and Case Western Reserve University School of Medicine, 10900 Euclid Avenue, BRB 425, Cleveland, Ohio 44106–4952, USA; cxf18@po.cwru.edu

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The beneficial effects of infliximab, the tumour necrosis factor antibody, in Crohn's disease may be mediated by apoptosis of activated mucosal T cells

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The advent of new biological agents for the treatment of autoimmune and chronic inflammatory disorders is drastically altering the approach to management while setting higher standards for therapeutic expectations. Only a fraction of the new biological agents keeps the promise of improved efficacy and specificity but the few that do can generate impressive results as we are currently witnessing for anti-tumour necrosis factor (TNF)- therapy in rheumatoid arthritis and Crohn's disease.^1,2 Based on these results, a number of other conditions where TNF- biological activity may play a pathogenic role, such as psoriasis, sarcoidosis, spondyloarthropathy, Behçet's syndrome, and sepsis, are being treated using TNF- blocking antibodies with variable but generally positive results. Since the first report of the use of infliximab in human disease,¹ the literature has swelled to over 200 publications on practical applications and theoretical considerations of this humanised antibody. In this enormous body of information . . . [Full text of this article]

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