Rheumatoid arthritis is a chronic destructive joint disease, mediated
by autoreactive immune cells. These cells, which express particular me
mbrane 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 r
eceptor, and adhesion molecules), human leucocyte antigen (HLA) class
II antigens. and cytokines (interleukin-1, tumour necrosis factor-alph
a and interleukin-6). Administration of rodent antibodies may cause im
mune 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 antibo
dies can only be made after more extensive experience. In particular,
there is an urgent need for double-blind controlled trials.