Fab-mediated binding of drug-dependent antibodies to platelets in quinidine- and quinine-induced thrombocytopenia.
TLDR
Findings suggest that binding of drug-induced antibodies to platelets occurs at the Fab domains of the IgG molecule.Abstract:
Platelets coated with quinine- or quinidine-induced antibodies form rosettes around protein A-Sepharose beads and normal platelets form rosettes about protein A-Sepharose beads coated with these antibodies. These reactions occurred only in the presence of sensitizing drug. Platelets also formed rosettes about protein A-Sepharose beads coated with an anti-PIA1 antibody, but drug was not required. Formation of rosettes between antibody-coated platelets and protein A-Sepharose was inhibited by F(ab')2 fragments of goat antibody specific for the Fc portion of human IgG, while rosette formation between antibody-coated protein A-Sepharose and platelets was inhibited by F(ab')2 fragments directed against the F(ab')2 portion of the IgG molecule. Since binding of IgG to protein A is known to occur via the Fc region, these findings suggest that binding of drug-induced antibodies to platelets occurs at the Fab domains of the IgG molecule.read more
Citations
More filters
Journal ArticleDOI
Mechanisms of Drug-Induced Immunologically Mediated Cytopenias
N. Raphael Shulman,Diane M. Reid +1 more
Journal ArticleDOI
11 Immunology of platelet disorders
TL;DR: The methodology for studying platelet antigens and antibodies involved in IMTPs has markedly improved in recent years, leading to better diagnostic tests but also to a better understanding of the immunopathogenesis of these diseases.
Journal ArticleDOI
Antimicrobial Drug-Induced Thrombocytopenia: A Review of the Literature
TL;DR: Clinicians should be vigilant in monitoring patient platelet counts, as an immune-mediated mechanism is frequently responsible for this hematologic adverse effect and is therefore unpredictable.
Journal ArticleDOI
Drug-induced Immune Thrombocytopenia
TL;DR: An overview of the different types of drug-induced thrombocytopenia is provided, potential pathologic mechanisms are discussed, and diagnostic methods and treatment options are considered.
Journal ArticleDOI
4 Bernard-Soulier syndrome
TL;DR: It is highly probable that the future study of platelets from patients with the Bernard-Soulier syndrome will further clarify the role of the GP Ib-IX complex in platelet physiology.
References
More filters
Journal ArticleDOI
A platelet and granulocyte membrane defect in paroxysmal nocturnal hemoglobinuria: usefulness for the detection of platelet antibodies
Richard H. Aster,Sara E. Enright +1 more
TL;DR: It is concluded that, in PNH, platelets and granulocytes share the membrane defect characteristic of erythrocytes in this disorder, and these observations support the concept that PNH arises as the result of a somatic mutation in a primitive cell capable of differentiating into ery Throttleblast, myeloblast, and megakaryoblast lines.
Journal ArticleDOI
Allergic purpura, including purpura due to foods, drugs and infections.
TL;DR: Purpura occurring during convalescence can best be explained on the assumption of an allergic basis, similar perhaps to that to which nephritis following streptococcal infections has been attributed.
Journal ArticleDOI
Immunoreactions involving platelets. I. A steric and kinetic model for formation of a complex from a human antibody, quinidine as a haptene, and platelets; and for fixation of complement by the complex.
TL;DR: Results of this study were consistent with the possibilities that the protein moiety of a haptenic antigen involved in development of an antibody which attaches to a cell is not necessarily a component of the cell, and that the cell reacts with the antibody by virtue of having a surface favorable for non-specific adsorption of certain haptene-antibody complexes.
Journal ArticleDOI
Cyclic AMP metabolism in cholesterol-rich platelets.
TL;DR: It is demonstrated that incorporation of cholesterol into platelet membranes is associated with a diminished inhibitory effect of prostaglandin E, on platelet aggregation and therefore adenosine 3’:5’-monophosphate production in these platelets.
Journal ArticleDOI
Drug-Antibody-Platelet Interaction in Quinine- and Quinidine-induced Thrombocytopenia
TL;DR: It is demonstrated that in quinine- and quinidine-induced thrombocytopenia, drug and antibody combine first in the soluble phase to form a complex, which then binds with high affinity to a receptor on the platelet surface (innocent bystander reaction), and that these antibodies are heterogeneous in respect to the amount of drug required to promote their binding to platelets, the number of platelet receptors they recognize, and their binding affinities.