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Investigation of the mechanisms of monoclonal antibody-induced platelet
activation
P Horsewood, CP Hayward, TE Warkentin and JG Kelton
Departments of Medicine, McMaster University Medical Centre, Hamilton,
Ontario, Canada.
Antiplatelet antibodies can activate platelets causing platelet aggregation
and the release reaction. However, the pathway of activation by these
antibodies is unknown and several potential mechanisms are possible. In
this report, we describe studies investigating potential pathways of
platelet activation by IgG antibodies. We tested 16 different IgG
monoclonal antibodies (MoAbs) against a variety of platelet surface
components and found that six antibodies were capable of causing platelet
aggregation and release. These included MoAbs against glycoprotein (GP)
IIb/IIIa, CD9, GPIV, and two other not well-characterized platelet
components. There was no relationship between the number of platelet
binding sites and the ability of an MoAb to activate the platelets. By
adding intact and F(ab')2 preparations of the MoAb to control or Fc
receptor-blocked platelets, we found that in all instances the MoAbs
initiated platelet activation via interacting with the platelet Fc
receptors. Clustering of the platelet protein components using a secondary
antibody did not cause activation. Studies into the pathway of Fc-dependent
activation demonstrated that the MoAbs were capable of activating platelets
by occupying Fc receptors on adjacent platelets (interplatelet activation),
as well as on the same platelet (intraplatelet activation).
Volume 78,
Issue 4,
pp. 1019-1026,
08/15/1991
Copyright © 1991 by The American Society of Hematology
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