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

The contribution of the pro-inflammatory macrophagederived cytokines IL-1 and tumor necrosis factor (TNF)-α has been well established through their capacity to modulate cartilage and bone metabolism. On the one hand, IL-1 and TNF-α stimulate osteoblasts to secrete cytokines such as granulocyte–monocyte colony stimulating factor (GM-CSF) and IL-6, which in turn regulate osteoclast formation. This leads, or not, to osteoclastic bone resorption according to the local conditions [4–6]. Chondrocyte activation similarly contributes to cartilage matrix destruction. On the other hand, IL-1 and TNF-α suppress matrix synthesis in cartilage and inhibit collagen synthesis in osteoblasts, leading to defective repair [7,8]. These two molecules are now, accordingly, the main targets for treatment, and the use of blocking anti-TNF-α antibodies, soluble TNF-α receptors and IL-1 receptor antagonist has shown very interesting clinical results, including protective effects on cartilage and bone [9–12].