Embracing novel cytokines in RA - complexity grows as does opportunity!
Current therapeutics for the treatment of rheumatoid arthritis (RA) offer limited efficacy in a restricted number of patients. There is, therefore, an unmet clinical need for the development of more efficacious therapeutics for the treatment of disease. Anti-TNFalpha therapy has provided proof of principle that cytokine blockade is an appropriate strategy by which to inhibit disease progression. In this review, we describe the basic biology of potential novel cytokine targets and the results of recent clinical trials, with particular focus on the cytokines related to Th17 biology, namely interleukin (IL)-12, IL-23 and IL-17, in addition to the TNF superfamily and the adipocytokines.
Hueber
Axel J
AJ
Centre for Rheumatic Diseases, Division of Immunology, Infection and Inflammation, 120 University Place Glasgow, G12 8TA, U.K.
Asquith
Darren L
DL
McInnes
Iain B
IB
Miller
Ashley M
AM
D054392:Adipokines / Q000037:antagonists & inhibitors* / Q000096:biosynthesis; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000276:immunology; D002986:Clinical Trials as Topic; D016207:Cytokines / Q000037:antagonists & inhibitors* / Q000096:biosynthesis; D015195:Drug Design; D006801:Humans; D020381:Interleukin-17 / Q000037:antagonists & inhibitors / Q000096:biosynthesis; D013583:Synovial Membrane / Q000187:drug effects / Q000378:metabolism; D058504:Th17 Cells / Q000187:drug effects* / Q000276:immunology; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000096:biosynthesis
D054392:Adipokines; D018501:Antirheumatic Agents; D016207:Cytokines; D020381:Interleukin-17; D014409:Tumor Necrosis Factor-alpha