Cytokines and direct cell contact in synovitis: relevance to therapeutic intervention.

摘要: In chronic inflammation, which leads to tissue destruction and fibrosis, immunocompetent cells migrate through the vascular endothelium target tissue. A prototype of these events is synovitis, occurs in diseases such as rheumatoid arthritis. The hypothesis that from bone marrow could also directly synovium channels interconnecting two compartments still under debate. Also, there no definitive answer regarding number result infiltration after migration, or proliferation at local site. Furthermore, survival synovitis being subjected some scrutiny, because evidence for a lack apoptosis pathological conditions. The interaction between lymphocytes different subsets monocyte/macrophages (type synovial cells) results production proinflammatory cytokines. These include interleukin (IL)-1 tumour necrosis factor (TNF)-α, induce connective B synoviocytes) produce large amounts matrix metallo-proteinases (MMPs), turn degrade extracellular components (eg collagens proteoglycans). Simultaneously, counter-regulatory mechanisms (cytokine inhibitors, anti-inflammatory cytokines protease inhibitors) are triggered an attempt block inflammation destruction. During, shortly onset chondrocytes bone-derived (osteoblasts osteoclasts) activated by same cytokines, together with prostanoids [mainly prostaglandin E2 (PGE2)], via MMPs remove mineral phase bone. inflammatory destructive process often followed attempts repair which, unfortunately, mostly fibrosis nonfunctional role TNF-α IL-1), growth factors has been extensively reviewed, and, owing particular concept inhibition TNF-α, crucial advances therapeutic intervention have made [1,2].