Platelet Satellitism Is FcγRIII (CD 16) Receptor–Mediated

Abstract

Platelet satellitism (PS), the phenomenon of platelet resetting around polymorphonuclear neutrophils (PMN), which is observed in ethylenediamineetetraacetic acid (EDTA)-anticoagulated blood at room temperature, is caused by the presence of IgG autoantibodies in the serum. Fourteen patients with PS were studied, and the presence of both EDTA-dependent antiplatelet and EDTA-dependent antineutrophil IgG (auto)antibodies were found in their sera. Anti-neutrophil activity was completely abolished when the sera were absorbed on normal platelets, which suggests that a single antibody is involved. Inhibition studies with monoclonal antibodies indicated that this IgG autoantibody is directed against the glycoprotein IIb/IIIa complex of the platelet membrane, as well as the neutrophil Fcγ receptor III (FcγRIII). In addition, the antibody did not react with platelets from a patient with type I Glanzmann’s disease, nor with neutrophils from a patient with congenital FcγRIII absence (NAnull phenotype), thus confirming both specificities. As in other literature cases, a clear correlation between the presence of this IgG and a specific clinical situation, disease, or use of drugs could not be shown. Therefore, these antibodies, which are present in some normal individuals, might occur naturally. Because of the exposure of particular cryptoantigenic structures present on EDTA-modified platelet and PMNs, they may manifest themselves by triggering the PS phenomenon.