An inflammatory lesion commonly develops in certain organs (e.g. skin, brain, kidneys and joints) either when antigen in the tissue spaces reacts with precipitating antibody forming microprecipitates in and around small blood vessels or when antigen in excess in the blood stream reacting with potentially precipitating antibody forms immune complexes (ICs) that lodge in the blood vessels. Other factors known to be essential for the pathogenesis of such lesions include (a) the activation of complement components, (b) chemotaxis towards ICs of PMN leucocytes and macrophages, (c) phagocytosis of ICs and (d) the formation and release by the phagocytes of prostaglandins, lysosomal enzymes, toxic metabolites of oxygen and other mediators of inflammation and tissue damage. Knowledge of these pathogenetic mechanisms opens up possibilities for chemotherapeutic attenuation or abolition of the development of antibody-dependent inflammatory lesions. The extent to which this goal has been achieved in the clinic with the aid of substances selected through the use of models of immune complex disease will be reviewed in this presentation.