Circulating immune complexes involving the ABO system after platelet transfusion

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Abstract
Summary. It has been proposed that when ABO unmatched platelets are transfused circulating immune complexes (CIC) may be formed between the patient's soluble ABH antigens and the transfused antibodies. Platelets might then be destroyed by bystander mechanisms or by the binding of CIC to the Fc receptor or to C3 binding membrane proteins on the platelet. An ELISA Clq assay was used to detect CIC in 40 patients with haematological diseases who had received multiple platelet transfusions. A significantly larger number of refractory patients were positive (41%) in the assay than non‐refractory patients (13%) or normal blood donors (0%). The presence of circulating IgG anti‐A was sought in six group A refractory patients who had been transfused with ABO unmatched platelets. To determine whether the IgG anti‐A was monomeric or in high molecular weight complexes, the serum was fractionated by gel exclusion chromatography and fractions were tested for the presence of IgG anti‐A. In all six patients the peak of IgG anti‐A binding occurred in fractions of high molecular weight (200–900 kD). Five out of six patients also demonstrated anti‐A activity in fractions corresponding to monomeric IgG (about 150–180 kD). Fractions containing high molecular weight anti‐A were purified using a protein G column and the eluates were tested for the presence of group A antigen using dot immunoblotting. Group A antigen was associated with the purified IgG anti‐A in 4/5 patients tested. Appropriate transfused and non‐transfused controls had no anti‐A in any fractions. Although not unexpected, these studies demonstrate for the first time that refractory patients receiving ABO unmatched platelets have CIC composed of ABO antigens and their corresponding antibodies present in their serum that circulate for at least several days. It also confirms the hypothesis that some CIC in haematological patients are induced by transfusion.