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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 α and β) than one (TNF-α). In his review article, Profess...
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2001
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC128897/ https://www.ncbi.nlm.nih.gov/pubmed/11438037 http://dx.doi.org/10.1186/ar302 |
Sumario: | 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 α and β) than one (TNF-α). In his review article, Professor Wim van den Berg argues that both TNF-α 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-α and IL-1 and suggests explanations of why TNF-α is a pivotal cytokine in this disease. |
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