Mediators of Inflammation

Mediators of Inflammation / 1994 / Article

Open Access

Volume 3 |Article ID 712943 | https://doi.org/10.1155/S0962935194000359

J. D. Sipe, J. Martel-Pelletier, I. G. Otterness, J.-P. Pelletier, "Cytokine Reduction in the Treatment of Joint Conditions", Mediators of Inflammation, vol. 3, Article ID 712943, 14 pages, 1994. https://doi.org/10.1155/S0962935194000359

Cytokine Reduction in the Treatment of Joint Conditions

Abstract

The destruction of joints caused by rheumatoid arthritis and osteoarthritis is characterized by an imbalance of enzyme catalysed cartilage breakdown and regeneration. A complex cytokine network perpetuates joint conditions by direct regulation of metalloproteases, by indirect recruitment of cells that secrete degradative enzymes, and by inhibition of reparative processes. The destructive action of cytokines such as interleukin-1, interleukin-6 and tumour necrosis factor-α can be modulated at multiple points associated either with cytokine production or with cytokine action. Potential agents for cytokine reduction include selective anti-cytokine antibodies, anticytokine receptor antibodies, cytokine receptor antagonist proteins, and soluble and chimeric cytokine receptor molecules. Pharmacologic regulation of IL-1 and TNFα remain primary targets for treatment of arthritis, and results of early clinical trials are promising. However, the results of long-term clinical trials will be required to support the value of anti-cytokine therapy in treatment of arthritis.

Copyright © 1994 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


More related articles

No related content is available yet for this article.
 PDF Download Citation Citation
 Order printed copiesOrder
Views259
Downloads393
Citations

Article of the Year Award: Outstanding research contributions of 2020, as selected by our Chief Editors. Read the winning articles.