We have previously identified non-HLA class I IgG alloantibodies that inhibit monocyte Fc-receptor function. They are involved in the protection of rhesus D-positive infants against red-cell destruction by maternal antibodies. We postulated that such antibodies may have potential therapeutic value for the treatment, prevention, or both of haemolytic disease in neonates and of various other antibody-mediated cytopenias. An experimental -globulin for intravenous administration was prepared from plasma containing such antibodies (monocyte-inhibiting -globulin, MIGG). As part of a prospective study, MIGG was given to a healthy man aged 31 years. He had no history of allergy, did not use medications, and had no febrile illness in the months before the study. The volunteer was typed for HLA (A26, A32, B39, B18 Cw7 DR4, DRw8 DRw52, DRw53 DQw3); serum immunoglobulin concentrations were normal. After the administration of 10 mL MIGG (0·6 g IgG; 0·5 mL/min) the volunteer started to complain of a dry cough and malaise. Manipulation of the infusion needle in his arm was followed by hypotension (decrease from 124/83 mm Hg to 108/67 mm Hg) with a slightly rapid pulse (increase from 61 beats/min to 74 beats/min) without other observable symptoms. The hypotension was mistakenly interpreted to be a vagal reaction. The patient recovered quickly and after 50 min the administration of MIGG was continued. 20 min later he started to cough again and suddenly became very ill with nausea, vomiting, and an increasing feeling of bodily discomfort. 80 mL MIGG (4·8 g IgG) had been infused. Blood pressure fell to 103/62 mm Hg and pulse rate rose to 110 beats/min. He started to produce white foamy sputum that soon became brown-coloured and tinged with blood. On auscultation, fine crepitations were audible at the bases of both lungs. Chest radiography showed diffuse bilateral pulmonary interstitial infiltration with a normal cardiac silhouette characteristic for non-cardiogenic pulmonary oedema (figure). Adult respiratory distress syndrome was suspected and the patient was started on intravenous hydrocortisone (200 mg). After 8 h he deteriorated and his blood pressure decreased further. He was intubated and received mechanical ventilation. Up to 100% oxygen and positive end-expiratory pressure up to 10 mm Hg were required during 4 days. Because the patient remained unstable, therapeutic leucapheresis combined with a 2·5 L plasmapheresis (exchanged with fresh-frozen plasma) procedure was done on day 3 in hospital. He improved clinically and the next day was extubated. We cannot, however, exclude coincidental improvement after this procedure. Subsequent recovery was complete and uneventful. Because