A follow-up to "Anti-cytokine therapy in chronic destructive arthritis" by Wim B van den Berg.
In recent years, the effectiveness of anti-TNF therapy in treating rheumatoid arthritis (RA) has become apparent. While trials of IL-1 receptor antagonist in RA have been encouraging, it clearly is more difficult to target two molecules (IL-1 alpha and beta) than one (TNF-alpha). In his review article, Professor Wim van den Berg argues that both TNF-alpha and IL-1 must be blocked in RA and that although TNF is clearly a potent inflammatory molecule, the dominant cytokine in the subsequent degradation of the joint tissue is IL-1. This commentary discusses his hypothesis in light of animal studies and the limitations of the conclusions that can be drawn from them. More broadly, it discusses the biology of TNF-alpha and IL-1 and suggests explanations of why TNF-alpha is a pivotal cytokine in this disease.
Brennan
F M
FM
Kennedy Institute of Rheumatology Division, Imperial College School of Medicine, Hammersmith, London, UK. f.brennan@ic.ac.uk
D000818:Animals; D000906:Antibodies / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000276:immunology / Q000628:therapy*; D002986:Clinical Trials as Topic; D004195:Disease Models, Animal; D006801:Humans; D007375:Interleukin-1 / Q000037:antagonists & inhibitors / Q000276:immunology*; D051379:Mice; D008822:Mice, Transgenic; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000276:immunology*
D000906:Antibodies; D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha