Simultaneous genotyping of human platelet antigen-1 to 17w by polymerase chain reaction sequence-based typing

Vox Sanguinis ◽  
2009 ◽  
Vol 97 (4) ◽  
pp. 330-337 ◽  
Author(s):  
X. Xu ◽  
F. Zhu ◽  
Y. Ying ◽  
S. Tao ◽  
Y. Liu ◽  
...  
1994 ◽  
Vol 4 (1) ◽  
pp. 15-19 ◽  
Author(s):  
S. Simsek ◽  
G. C. L. M. Christiaens ◽  
H. H. H. Kanhai ◽  
J. R. Beekhuis ◽  
P. M. M. Bleeker ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-5 ◽  
Author(s):  
Shun-Chung Pai ◽  
Thierry Burnouf ◽  
Jen-Wei Chen ◽  
Liang-In Lin

Polymorphism of human platelet antigens (HPAs) leads to alloimmunizations and immune-mediated platelet disorders including fetal-neonatal alloimmune thrombocytopenia (FNAIT), posttransfusion purpura (PTP), and platelet transfusion refractoriness (PTR). HPA typing and knowledge of antigen frequency in a population are important in particular for the provision of HPA-matched blood components for patients with PTR. We have performed allele genotyping for HPA-1 through -6 and -15 among 998 platelet donors from 6 blood centers in Taiwan using sequence-specific primer polymerase chain reaction. The HPA allele frequency was 99.55, and 0.45% for HPA-1a and -1b; 96.49, and 3.51% for HPA-2a and -2b; 55.81, and 44.19% for HPA-3a and -3b; 99.75, and 0.25% for HPA-4a and -4b; 98.50, and 1.50% for HPA-5a and -5b; 97.75 and 2.25% for HPA-6a and -6b; 53.71 and 46.29% for HPA-15a and -15b. HPA-15b and HPA-3a, may be considered the most important, followed by HPA-2, -6, -1, -5, and -4 systems, as a cause of FNAIT, PTP, and PTR based on allele frequency. HPA-4b and HPA-5b role cannot be excluded based on their immunogenicity. A larger-scale study will now be conducted to confirm these hypotheses and to establish an apheresis donor database for the procurement of HPA-matched apheresis platelets for patients with PTR.


1993 ◽  
Vol 69 (05) ◽  
pp. 485-489 ◽  
Author(s):  
Isabelle Djaffar ◽  
Didier Vilette ◽  
Dominique Pidard ◽  
Jean-Luc Wautier ◽  
Jean-Philippe Rosa

SummaryThe human platelet antigen (HPA) 3 system is expressed on GPIIb, one subunit of GPIIb-IIIa, the platelet fibrinogen receptor. It was recently shown that HPA-3 was associated with an Ile843/Ser polymorphism. To investigate further HPA-3 determinant structure, we localized an HPA-3a determinant, recognized by the alloantiserum Leka, within the last 29 amino acids of GPIIbα. This region encompasses the polymorphic Ile843, which, as expected, is substituted into Ser in Leka-negative individuals, as shown by DNA sequence after polymerase chain reaction on platelet RNA. In addition, contribution of glycosylation to the determinant structure was demonstrated since the Leka antigenicity was strongly decreased after specifically removing nonterminal O-linked sugars, but not terminal sialic acids. We have thus refined the localization of an HPA-3a determinant within the last 29 amino acids, including Ile843, of GPIIb heavy chain, and shown that the Leka HPA-3a determinant is dependent, in part, upon the serine-linked carbohydrates adjacent to Ile/Ser843.


2011 ◽  
Vol 78 (3) ◽  
pp. 226-227 ◽  
Author(s):  
F.-M. Zhu ◽  
W. Wang ◽  
W. Zhang ◽  
H.-J. Lv ◽  
L.-X. Yan

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