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Anti‐HPA1a antibodies induce CD62P and fibrinogen binding
Author(s) -
Koren D.,
Janisiw M.,
Eichelberger B.,
Panzer S.
Publication year - 2000
Publication title -
transfusion medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.471
H-Index - 59
eISSN - 1365-3148
pISSN - 0958-7578
DOI - 10.1046/j.1365-3148.2000.00261-19.x
Subject(s) - platelet , cd63 , fibrinogen , chemistry , antibody , flow cytometry , microbiology and biotechnology , platelet membrane glycoprotein , antiserum , antigen , platelet activation , immunology , biology , biochemistry , microrna , microvesicles , gene
B ackground Alloantibodies to platelet antigens may affect platelet function by delivering stimulatory or inhibitory signals or by occupying platelet receptor‐ligand molecules. So far, reports from the literature are controversial. M ethods We investigated CD62P and CD63 expression, as well as fibrinogen‐binding on platelets that have been incubated with sera containing anti‐HPA‐1a (NAIT, n = 11; PTP, n = 5) by flow cytometry. HPA‐1a/a platelets from HLA‐matched donors were incubated with antisera and then stimulated with TRAP‐6 (20 µ m and 50 µ m ) to study stimulatory or inhibitory effects. R esults NAIT: TRAP‐6 20 µ m and 50 µ m induced CD62P expression was enhanced by 2 and 4 sera, respectively. Fibrinogen binding was induced by 6 sera and enhanced if with TRAP‐6 20 µ m and 50 µ m by 3 and 8 sera, respectively. PTP: 2 sera induced CD62P and all 5 augmented its TRAP‐6 50 µ m induced expression. Fibrinogen binding was induced by 4 sera and all 5 sera enhanced its TRAP‐6 50 µ m induced binding. There were no changes in the CD63 expression. C onclusion s HPA‐1a antibodies activate platelets to release CD62P and support fibrinogen binding. These effects are stronger in PTP than in NAIT.