Skip to main content
U.S. flag

An official website of the United States government

This site is currently in beta, and your feedback is helping shape its ongoing development.

IL-17 derived from juxta-articular bone and synovium contributes to joint degradation in rheumatoid arthritis

Published by National Institutes of Health | U.S. Department of Health & Human Services | Metadata Last Checked: September 07, 2025 | Last Modified: 2025-09-06
The origin and role of IL-17, a T-cell derived cytokine, in cartilage and bone destruction during rheumatoid arthritis (RA) remain to be clarified. In human ex vivo models, addition of IL-17 enhanced IL-6 production and collagen destruction, and inhibited collagen synthesis by RA synovium explants. On mouse cartilage, IL-17 enhanced cartilage proteoglycan loss and inhibited its synthesis. On human RA bone explants, IL-17 also increased bone resorption and decreased formation. Addition of IL-1 in these conditions increased the effect of IL-17. Blocking of bone-derived endogenous IL-17 with specific inhibitors resulted in a protective inhibition of bone destruction. Conversely, intra-articular administration of IL-17 into a normal mouse joint induced cartilage degradation. In conclusion, the contribution of IL-17 derived from synovium and bone marrow T cells to joint destruction suggests the control of IL-17 for the treatment of RA.

Find Related Datasets

Click any tag below to search for similar datasets

data.gov

An official website of the GSA's Technology Transformation Services

Looking for U.S. government information and services?
Visit USA.gov