Blood group A and B antigens are strongly expressed on platelets of some individuals

Abstract

It is widely thought that expression of ABH antigens on platelets is insufficient to materially affect the survival of ABH-incompatible platelets in transfusion recipients, but anecdotal reports of poor survival of A and B mismatched platelets suggest that this is not always the case. The A and B antigen expression on platelets of 100 group A1 and group B blood donors was measured, and 7% and 4%, respectively, had platelets whose A and B antigen levels consistently exceeded the mean plus 2 SD. On the basis of flow cytometric and statistical analysis, donors whose platelets contained higher than normal levels of A antigen were subdivided into 2 groups, designated Type I and Type II (“high expressers”). Serum A1- and B-glycosyltransferase levels of A and B high expressers were significantly higher than those of group A1 and B individuals with normal expression. H antigen levels were low on the red cells of high expressers, indicating that the anomaly affects other cell lineages. Immunochemical studies demonstrated high levels of A antigen on various glycoproteins (GPs) from high-expresser platelets, especially GPIIb and PECAM (CD31). The A1 Type II high-expresser phenotype was inherited as an autosomal dominant trait in one family. The sequences of exons 5, 6, and 7 of the A1-transferase gene of one Type II A1 high expresser and exon 7 from 3 other genes were identical to the reported normal sequences. Further studies are needed to define the molecular basis for the high-expresser trait and to characterize its clinical implications.

Relationship betweenABOgenotype andAantigen expression on platelets

“…Clinically, our findings are of interest to PLT transfusion support. As observed in prior reports, group A individuals lacking the A 1 allele expressed the A antigen only weakly on PLTs. The A antigen MFI among A 2 /O , A 2 /A 2 , and A 2 B individuals (mean, 159 ± 131) was slightly greater than the background MFI seen among group O subjects (mean, 63 ± 32), providing laboratory evidence to support the use of PLTs from A 1 ‐negative donors as a substitute for group O donor PLTs during transfusion support of group O or group B recipients.…”

“…In agreement with others, we found that H antigen was much more strongly expressed than A antigen on PLTs. In contrast with RBCs where H expression is inversely related to A expression, Curtis and coworkers, Cooling and coworkers, and Sant'Anna Gomes and coworkers reported that on PLTs increasing H antigen was directly related to increasing A antigen, a result we also observed among A 1 /A 1 individuals, but not among A 1 /O persons. As reported by Le Pendu and colleagues, Ogasawara and colleagues, and Cooling and colleagues, we also found that A antigen expression was not related to secretor status.…”

“…These studies identified high‐expresser variants first recognized by Ogasawara and colleagues . Previous reports by Curtis and colleagues, Cooling and colleagues, and Sant'Anna Gomes and colleagues have characterized A and H antigen expression on PLTs. The purpose of our study was to extend these observations by correlating antigen expression with ABO genotype.…”

New platelet glycoprotein polymorphisms causing maternal immunization and neonatal alloimmune thrombocytopenia

“…Blood types of fathers were A 1 (Sey) and A 2 B (Hug). Because high‐titer IgG maternal antibodies specific for blood groups A or B can cause neonatal thrombocytopenia in infants who possess a genetic trait that causes PLTs to express many times the normal levels of A or B antigens, 12,19 the maternal sera were absorbed with washed group A 1 and B red blood cells. This treatment had no effect on the reactions with paternal PLTs.…”

“…Maternal samples from suspected NAIT cases were tested against paternal PLTs and PLTs from group O donors of known phenotypes using flow cytometry as previously described 10‐12 . Antibodies reactive with GPIIb/IIIa, GPIb/IX, GPIa/IIa, and GPIV were detected by direct and modified antigen‐capture enzyme‐linked immunosorbent assay (ELISA, ACE, and MACE) 10 …”