The majority of cytokines that are detected in the infl amed joints of patients of RA function as proinfl ammatory mediators, promoting the infl ammatory process as well as cartilage and bone destruction. In addition, anti-infl ammatory cytokines and molecules are detected in the joints, but in active disease their levels are too low to inhibit the deleterious effects of proinfl ammatory cytokines. The role of individual cytokines in the pathogenesis of RA has been investigated by studying their expression in RA, and by studying the effects of cytokines and their inhibitors on synovial cells in vitro, on animal models of arthritis and, more recently, on disease activity in patients with RA. Tumor necrosis factor (TNF) is a proinfl ammatory cytokine with multiple effects on the cells of the immune system as well as on cartilage and bone. Importantly, it regulates the production of other proinfl ammatory mediators in the joints. Both preclinical and clinical studies indicate TNF as a key cytokine in the pathogenesis of RA, and different anti-TNF agents are now widely used to treat patients with active disease. Interleukin
Department of Internal Medicine, Division of Rheumatology, Tampere University Hospital, Biokatu 6, 33520 Tampere, Finland and Institute of Biomedical Technology, Tampere University; Email: firstname.lastname@example.org List of abbreviations after the text.