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IL-17 derived from juxta-articular bone and synovium contributes to joint degradation in rheumatoid arthritis
Authors:Martine Chabaud  Erik Lubberts  Leo Joosten  Wim van den Berg  Pierre Miossec
Affiliation:1. INSERM U403, Faculté de Médecine Laennec, and Departments of Immunology and Rheumatology, H?pital Edouard Herriot, Lyon, France
2. Rheumatology Research Laboratory, Department of Rheumatology, University Hospital Nijmegen, HB Nijmegen, The Netherlands
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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