Rheumatoid arthritis (RA) is an autoimmune disease characterized by acute and chronic inflammation of the synovial joints causing destruction and loss of function. The etiology of RA is unknown. Cytokines, as essential signal molecules in inflammation, are known to be involved in the pathogenesis of RA:

• Vasculitis with recruitment and activation of cytokine-producing inflammatory cells, including monocytes / macrophages, T- and B-lymphocytes, and neutrophils, are characteristically found in affected tissues.
• Inflammatory cytokines such as IL-1 and TNF are found in increased amounts in the affected tissues, in synovial fluids of affected joints, and in the circulation of RA patients.
• IL-1 and TNF induce arthritis resembling RA in experimental animals.
• Experimental arthritis induced f.ex. by mycobacteria is prevented by neutralising IL-1 and TNF.
• The effects of IL-1 and TNF on synovial cells, fibroblasts, bone cells (osteoblasts and osteoclasts) and chondrocytes are all compatible with the pathophysiology of RA.
• TNFa transgenic mice develop arthritis, and this is prevented by anti-TNF antibody therapy; TNFa induces IL-1 in many cells.
• Striking beneficial effects can be obtained by treatment of RA patients with anti-TNF monoclonal antibodies.

Rheumatoid arthritis (RA) is a systemic autoimmune disease characterised by severe inflammation in many joints. The inflammatory process forms an invasive pannus, which in many cases leads to cartilage and joint destruction. Many forms of arthritis, including RA, are currently incurable, leading to crippling disease in as many as 1-2% of the World's population.