Cytokine Reduction in the Treatment of Joint Conditions
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 th...
Saved in:
| Main Authors: | , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wiley
1994-01-01
|
| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/S0962935194000359 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| Summary: | 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. |
|---|---|
| ISSN: | 0962-9351 1466-1861 |