AbstractDexamethasone-21-phosphate (Dex-21-P) was encapsulated in human erythrocytes by a procedure of hypotonic hemolysis and isotonic resealing in a wide range of concentrations (0.2 to 8.5 mm). The erythrocyte membrane was then modified by the addition of Zn and bis(sulfosuccinimidyl)suberate inducing the formation of stable antigenic sites that are recognized by autologous immunoglobulins with subsequent complement deposition (C3b). Dexamethasone-21-phosphateloaded erythrocytes, modified as above, are readily recognized by macrophages through their Fe and C3b receptors with consequent phagocytosis and delivery of Dex-21-P from erythrocytes to the macrophages. In vitro targeting of Dex-21-P-loaded erythrocytes to human monocyte-derived macrophages was found to re-duce by more than 60% the phorbol 12-myristate 13-acetate-stimulated O2- release. Thus, the targeting of glucocorticoids to macrophages is feasible and results in the inhibition of respiratory burst.