[Rheumatoid polyarthritis. Immunopathological mechanisms, contribution of experimental arthritis]

Rheumatoid arthritis is an auto-immune disease the autoantigen of which has not yet been identified. Induction and maintenance of the disease may involve environmental factors (bacteria, viruses) and autoantigens directly issued from the articular tissue (collagens, proteoglycans). T cells play a crucial role in rheumatoid arthritis; after the antigen has been recognized, they secrete lymphokines and enable other T and B lymphocytes to be activated. The synovial cells themselves can produce large amounts of lymphokines and enzymes which contribute to the destruction of joints. The immunopathology of rheumatoid arthritis is now much better known owing to studies of experimental arthritis which are the animal models of the disease. These models have helped in validating therapeutic approaches based on immunointervention.