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)-α therapy in rheumatoid arthritis and Crohn's disease.^1,2 Based on these results, a number of other conditions where TNF-α biological activity may play a pathogenic role, such as psoriasis, sarcoidosis, spondyloarthropathy, Behçet's syndrome, and sepsis, are being treated using TNF-α 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 however, disappointingly little is found on the mechanisms of action of infliximab. Almost invariably the optimism caused by the feeling of finally having discovered a magic bullet against unyielding diseases causes all interest and resources to be shifted to more clinical trials. Although this reaction is understandable, all too often it comes at the expense of investigating mechanisms of action that would ultimately lead to a safer and more reliable use of the biological agent, or even the discovery of better biologicals. Thus the study of ten Hove et …