ABSTRACT
Advances in the understanding of basic disease mechanisms in rheumatoid arthritis (RA) are leading to the development of new, rational therapies. In one widely accepted view of disease pathogenesis, RA is initiated and possibly maintained by an immune response involving the recognition by T cells of an autoantigen (yet uncharacterized) in the context of a specific "shared epitope" HLA-DR~ gene product (l ), with consequent T-cell activation and the initiation of an inflammatory cascade. Although cytokines may be involved in the initiating immune response, they are particularly important in the subsequent processes of inflammation and it is to this level that anticytokine therapy is primarily directed.
