Fc‐receptor (FcR)‐mediated phagocytosis and FcR (FcRI, FcRII and FcRIII) membrane expression was studied on freshly separated and cultured monocyles (Mo) from 20 AIDS patients and 20 healthy controls. Both Mo and Mo‐derived macrophages from AIDS patients presented a significant defect in their capacity to ingest IgG‐coated erythrocytes (EA) compared to control cells. This functional defect did not depend on a decline in the n umber of FcR+cells or on a decrease in the expression of FcR on their surface. In fact, the percentages of phagocytes reacting with anti‐FcRI Mo Ab (32.2) or ami‐FcR II MoAb (IV. 3) were similar for controls and AIDS patients, while the percentage of FcRIII‐positive Mo (MoAb 3G8) was higher in the AIDS population than in controls, though this difference was not seen on cultured Mo. The level of FcRI expression, evaluated as mean fluorescence intensity (MFI), was higher on freshly separated Mo from AIDS patients than from controls but this difference disappeared also with differentiation of Mo to Mo‐derived macrophagesin vitro. Parallel analysis of FcRII and FcRIII onphagocytes revealed no differences in the MFI between the AIDS and control groups. Some observations suggested that this functional defect might be secondary to phagocyte priming by circulating lFN‐γ: (1)in vitrostimulation of Mo with hrIFN‐γ, which increased FcRI expression, actually reduced phagocytosis of IgG‐coated particles; and (2) IFN‐γ concentrations were increased in AIDS patients' plasma. In spite of these findings, no significant correlation was found between plasma IFN‐γ concentrations and FcR‐mediated ingestion in AIDS patients, making the hypothesis uncertain. Even if the basis for the impaired FcR‐mediated phagocytosis in AIDS patients remains unclear, this functional defect may have a role in the immunopathogenesis of AIDS, constituting a compon