Rheumatoid arthritis is a chronic destructive joint disease, mediated by autoreactive immune cells. These cells, which express particular membrane antigens and release proliferative and catabolic cytokines, can be targeted by monoclonal antibodies. Potential targets for specific immune intervention with monoclonal antibodies are lymphocyte membrane antigens (CD3, CD4, CD5, CD7, CDw52, interleukin-2 receptor, T cell receptor, and adhesion molecules), human leucocyte antigen (HLA) class II antigens, and cytokines (interleukin-1, tumour necrosis factor-α and interleukin-6).
Administration of rodent antibodies may cause immune reactions. To minimise these, it is preferable to use humanised (chimaeric or complementarity-determining region-grafted) antibodies.
A final judgement on the clinical usefulness of these monoclonal antibodies can only be made after more extensive experience. In particular, there is an urgent need for double-blind controlled trials.