PLATELET SATELLITISM IS FC-GAMMA-RIII (CD16) RECEPTOR-MEDIATED

Citation
N. Bizzaro et al., PLATELET SATELLITISM IS FC-GAMMA-RIII (CD16) RECEPTOR-MEDIATED, American journal of clinical pathology, 103(6), 1995, pp. 740-744
Citations number
21
Categorie Soggetti
Pathology
ISSN journal
00029173
Volume
103
Issue
6
Year of publication
1995
Pages
740 - 744
Database
ISI
SICI code
0002-9173(1995)103:6<740:PSIF(R>2.0.ZU;2-8
Abstract
Platelet satellitism (PS), the phenomenon of platelet resetting around polymorphonuclear neutrophils (PMN), which is observed in ethylenedia mineetetraacetic acid (EDTA)-anticoagulated blood at room temperature, is caused by the presence of Ige autoantibodies in the serum. Fourtee n patients with PS were studied, and the presence of both EDTA-depende nt antiplatelet and EDTA-dependent antineutrophil IgG (auto)antibodies were found in their sera, Anti-neutrophil activity was completely abo lished when the sera were absorbed on normal platelets, which suggests that a single antibody is involved. Inhibition studies with monoclona l antibodies indicated that this IgG autoantibody is directed against the glycoprotein IIb/IIIa complex of the platelet membrane, as well as the neutrophil Fc gamma receptor III(Fc gamma RIII). In addition, the antibody did not react with platelets from a patient with type I Glan zmann's disease, nor with neutrophils from a patient with congenital F c gamma RIII absence (NAnull phenotype), thus confirming both specific ities. As in other literature cases, a clear correlation between the p resence of this IgG and a specific clinical situation, disease, or use of drugs could not be shown. Therefore, these antibodies, which are p resent in some normal individuals, might occur naturally. Because of t he exposure of particular cryptoantigenic structures present on EDTA-m odified platelet and PMNs, they may manifest themselves by triggering the PS phenomenon.