[HTML][HTML] IL-17 derived from juxta-articular bone and synovium contributes to joint degradation in rheumatoid arthritis
M Chabaud, E Lubberts, L Joosten… - Arthritis Research & …, 2001 - Springer
M Chabaud, E Lubberts, L Joosten, W van den Berg, P Miossec
Arthritis Research & Therapy, 2001•SpringerThe 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 …
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 …
Abstract
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.
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