PLTs of Blood Group A₁ donors express increased surface A antigen owing to apheresis and prolonged storage

Abstract

Apheresis and prolonged storage of A1 group PCs independently led to overexpression of A antigen on the PLT surface. This may make such PCs more susceptible to destruction by anti-A of O or B group recipients.

Expression of ABH antigens on platelets

“…Similar reactions were obtained with MoAb BRIC-198. Findings made with both probes confirm our previous observations that groups A 2 and O platelets carry about the same amount of H antigen and that overexpression of A is associated with markedly decreased levels of H. 2 The alpha-2-fucosyltransferase responsible for the synthesis of H and the glycosyltransferases responsible for the synthesis of A and B antigens (including A 2 ) are encoded at distinct loci on different chromosomes. It would be most unexpected for the H-transferase gene to be selectively inactivated in megakaryocytes of persons with the A 2 red cell phenotype.…”

“…1 An accompanying commentary noted surprise that the thiopurine methyltransferase (TPMT) genotype was not predictive of relapse risk. 2 The answer may lie in the fact that the starting dose of mercaptopurine (75 mg/m 2 per day) in our study was higher than some groups use, and that therapy was individualized based on TPMT status.…”

“…Both observations conflict with our previous report showing that A 2 and O platelets carry comparable amounts of H antigen and that H expression on platelets, as on red cells, is inversely related to expression of A antigen. 2 In our studies, we used an H-specific monoclonal antibody (MoAb) BRIC-198, whereas Cooling et al used FITClabeled Ulex europaeus lectin to quantify platelet H antigen by flow cytometry. To check whether these 2 H-specific probes might yield different results, we obtained FITC-labeled Ulex from the same source as Cooling et al (Sigma, St Louis, MO) and examined its reactions against platelets using 2-color flow cytometry and washed platelets of different phenotypes isolated by differential centrifugation.…”

“…The need to avoid platelet activation to study circulating platelets cannot be overemphasized. Platelet activation can dramatically alter platelet 2,3 Studies by Julmy et al have shown a 50% increase in ABH on A 1 platelets following platelet activation. 2 The mechanism surrounding this phenomenon is poorly understood, but may involve a combination of altered glycoprotein expression following alpha granule translocation and microparticle shedding.…”

Determinants of ABH expression on human blood platelets

“…Risk factors in the recipient can include a group O phenotype and unusually high levels of anti-A and anti-B isohemagglutinins. 8,9,12,[16][17][18] Donor and/or platelet factors are less well described but may include storage time, [19][20][21] and Lewis and ABO subtypes. 2,4,5,8,[22][23][24] In addition, an ABH-high expresser (ABH-HXP) platelet phenotype has been identified that is specifically linked to transfusion failures.…”