Chemokine inhibition in inflammatory arthritis.
Synovial inflammation in rheumatoid arthritis (RA) and other arthritides is, in part, dependent on migration of inflammatory cells as well as retention of these cells at the site of inflammation. Chemokines play a critical role in these processes and represent an attractive target for therapeutic intervention. Animal models of RA have shown that it is possible to induce clinical improvement by specifically targeting chemokines or their receptors. Although at present only very limited data exist, initial data suggest that it may be possible to reduce synovial inflammation in patients with RA by specific chemokine blockade. Innovative trial design may help to screen for potentially interesting chemokine antagonists in an early stage of development.
Tak
Paul P
PP
Division of Clinical Immunology and Rheumatology F4-218, Academic Medical Centre/University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands. p.p.tak@amc.uva.nl
D000818:Animals; D001168:Arthritis / Q000188:drug therapy* / Q000276:immunology; D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000276:immunology; D018925:Chemokines / Q000378:metabolism; D006801:Humans; D008264:Macrophages / Q000502:physiology; D054390:Receptors, CCR2; D019707:Receptors, Chemokine / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D013583:Synovial Membrane / Q000187:drug effects / Q000276:immunology
C515334:CCR2 protein, human; D018925:Chemokines; D054390:Receptors, CCR2; D019707:Receptors, Chemokine