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- W36901207 abstract "BackgroundHeparin‐induced thrombocytopenia (HIT) is an adverse drug reaction that results in thrombocytopenia and, in some patients, thrombotic complications. HIT is mediated by antibodies that bind to complexes of platelet factor 4 (PF4) and heparin. The antigenic epitopes of these anti‐PF4/heparin antibodies have not yet been precisely defined, because of the polyspecific immune response that characterizes HIT.To identify PF4 amino acids essential for binding pathogenic HIT antibodies.Alanine scanning mutagenesis was utilized to produce 70 single point mutations of PF4. Each PF4 mutant was used in an enzyme immunoassay (EIA) to test their capacity to bind a platelet‐activating murine monoclonal anti‐PF4/heparin antibody (KKO) and HIT patient sera (n = 9).We identified 13 amino acids that were essential for binding KKO because they directly affected either the binding site or the antigenic conformation of PF4. We also identified 10 amino acids that were required for the binding of HIT patient sera and five of these amino acids were required for binding both KKO and the HIT patient sera. The 10 amino acids required for binding HIT sera were further tested to differentiate pathogenic HIT antibodies (platelet activating, n = 45) and non‐pathogenic antibodies (EIA‐positive but not platelet activating, n = 28). We identified five mutations of PF4 that were recognized to be essential for binding pathogenic HIT antibodies. Using alanine scanning mutagenesis, we characterized possible binding sites of pathogenic HIT antibodies on PF4." @default.
- W36901207 created "2016-06-24" @default.
- W36901207 creator A5002544827 @default.
- W36901207 creator A5047037554 @default.
- W36901207 date "1978-10-01" @default.
- W36901207 modified "2023-10-10" @default.
- W36901207 title "Thrombocytopenia: Mechanisms and Management of Defects in Platelet Production" @default.
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- W36901207 doi "https://doi.org/10.1016/s0308-2261(21)00047-3" @default.
- W36901207 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/363326" @default.
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