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Journal articles on the topic 'Human platelet antigens'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Kao, KJ, DJ Cook, and JC Scornik. "Quantitative analysis of platelet surface HLA by W6/32 anti-HLA monoclonal antibody." Blood 68, no. 3 (September 1, 1986): 627–32. http://dx.doi.org/10.1182/blood.v68.3.627.627.

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Abstract Class I molecules of human major histocompatibility complex (HLA) are the most important antigenic system in determining the survival of transfused platelets in alloimmunized patients. Platelets with reduced expression of a specific type of HLA antigen may escape specific anti- HLA antibody-mediated destruction. By using 125I-labeled Fab fragments of W6/32 anti-HLA monoclonal antibody and competitive protein binding assays, we measured the range of total HLA concentrations on platelets. In 12 individuals examined, the mean number of HLA-A, B, and C molecules per platelet was 81,587 +/

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2

Kao, KJ, DJ Cook, and JC Scornik. "Quantitative analysis of platelet surface HLA by W6/32 anti-HLA monoclonal antibody." Blood 68, no. 3 (September 1, 1986): 627–32. http://dx.doi.org/10.1182/blood.v68.3.627.bloodjournal683627.

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Class I molecules of human major histocompatibility complex (HLA) are the most important antigenic system in determining the survival of transfused platelets in alloimmunized patients. Platelets with reduced expression of a specific type of HLA antigen may escape specific anti- HLA antibody-mediated destruction. By using 125I-labeled Fab fragments of W6/32 anti-HLA monoclonal antibody and competitive protein binding assays, we measured the range of total HLA concentrations on platelets. In 12 individuals examined, the mean number of HLA-A, B, and C molecules per platelet was 81,587 +/- 20,016

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3

Curtis, B. R., and J. G. McFarland. "Human platelet antigens - 2013." Vox Sanguinis 106, no. 2 (September 16, 2013): 93–102. http://dx.doi.org/10.1111/vox.12085.

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4

Cooling, Laura L. W., Kathleen Kelly, James Barton, Debbie Hwang, Theodore A. W. Koerner, and John D. Olson. "Determinants of ABH expression on human blood platelets." Blood 105, no. 8 (April 15, 2005): 3356–64. http://dx.doi.org/10.1182/blood-2004-08-3080.

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AbstractPlatelets express ABH antigens, which can adversely effect platelet transfusion recovery and survival in ABH-incompatible recipients. To date, there has been no large, comprehensive study comparing specific donor factors with ABH expression on platelet membranes and glycoconjugates. We studied ABH expression in 166 group A apheresis platelet donors by flow cytometry, Western blotting, and thin layer chromatography relative to donor age, sex, A1/A2 subgroup, and Lewis phenotype. Overall, A antigen on platelet membranes, glycoproteins, and glycosphingolipids was linked to an A1 red blood

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5

Guo, Li, Sikui Shen, Jesse W. Rowley, Neal D. Tolley, Wenwen Jia, Bhanu Kanth Manne, Kyra N. McComas, et al. "Platelet MHC class I mediates CD8+ T-cell suppression during sepsis." Blood 138, no. 5 (April 25, 2021): 401–16. http://dx.doi.org/10.1182/blood.2020008958.

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Abstract Circulating platelets interact with leukocytes to modulate host immune and thrombotic responses. In sepsis, platelet-leukocyte interactions are increased and have been associated with adverse clinical events, including increased platelet–T-cell interactions. Sepsis is associated with reduced CD8+ T-cell numbers and functional responses, but whether platelets regulate CD8+ T-cell responses during sepsis remains unknown. In our current study, we systemically evaluated platelet antigen internalization and presentation through major histocompatibility complex class I (MHC-I) and their eff

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6

Athanasou, N. A., J. Quinn, A. Heryet, and J. O. McGee. "Localization of platelet antigens and fibrinogen on osteoclasts." Journal of Cell Science 89, no. 1 (January 1, 1988): 115–22. http://dx.doi.org/10.1242/jcs.89.1.115.

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The antigenic phenotype of the human osteoclast, which is known to be derived from a circulating mononuclear precursor cell of haemopoietic origin, is controversial. Recent studies have shown that macrophage as well as megakaryocyte/platelet antigens are expressed by osteoclasts. In this study, we have sought to define, by immunohistochemistry, the nature and possible function of platelet antigens expressed by human osteoclasts in foetal and adult bone specimens. Monoclonal antibodies to platelet glycoprotein IIIa (gpIIIa) and CD9 antibodies stained osteoclasts in all bone specimens examined.

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7

Metcalfe, P., N. A. Watkins, W. H. Ouwehand, C. Kaplan, P. Newman, R. Kekomaki, M. de Haas, et al. "Nomenclature of human platelet antigens." Vox Sanguinis 85, no. 3 (October 2003): 240–45. http://dx.doi.org/10.1046/j.1423-0410.2003.00331.x.

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8

Wen, Ying-hao, and Ding-Ping Chen. "Human platelet antigens in disease." Clinica Chimica Acta 484 (September 2018): 87–90. http://dx.doi.org/10.1016/j.cca.2018.05.009.

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9

Thurlow, P. J., L. Kerrigan, R. A. Harris, and I. F. McKenzie. "Analysis of human bone marrow with monoclonal antibodies." Journal of Histochemistry & Cytochemistry 33, no. 12 (December 1985): 1183–89. http://dx.doi.org/10.1177/33.12.2415573.

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In order to study the antigenic phenotype of different hemopoietic cells, we used a series of monoclonal antibodies to investigate normal bone marrow in a standard immunofluorescence assay. The antibodies detected the following antigens: HLA-ABC, beta 2-microglobulin (beta 2m), HLA-DR (Ia), a lymphocyte subset and specific antigen (T and B) HuLy-m2, m3, T lymphocyte antigen (HuLy-m1), lymphocyte T200 antigen (HuLy-m4), a viral-associated antigen (HuLy-m5), and platelet-specific glycoproteins IIb-IIIa (HuPl-m1). The following results were obtained: (a) normoblasts were weakly HLA-ABC+, beta 2m+

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10

Enomoto, Takayuki, Hisako Maruoka, Sumio Hanagaki, Shoji Morita, Masuhiro Shimamura, Keiichi Hando, Ayako Ishijima, et al. "Pregnancy-induced Alloimmunization against Platelet Antigens. HLA and Human Platelet Antigens (HPA)." Journal of the Japan Society of Blood Transfusion 46, no. 5 (2000): 467–73. http://dx.doi.org/10.3925/jjtc1958.46.467.

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11

De Reys, S., C. Blom, B. Lepoudre, PJ Declerck, M. De Ley, J. Vermylen, and H. Deckmyn. "Human platelet aggregation by murine monoclonal antiplatelet antibodies is subtype-dependent." Blood 81, no. 7 (April 1, 1993): 1792–800. http://dx.doi.org/10.1182/blood.v81.7.1792.1792.

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Abstract Twenty murine monoclonal antibodies (MoAbs) generated against different human platelet antigens induced clumping of human platelets in plasma and buffer. Whereas one MoAb could agglutinate platelets, clumping for 19 MoAbs was blocked by metabolic inhibitors, indicating that these induce platelet activation. Fifteen MoAbs were of IgG1, two of IgG2a, and two of IgG2b subtype. F(ab')2 fragments of these did not evoke an aggregatory response, but specifically inhibited aggregations by and binding of their respective intact MoAbs to platelets. Single-platelet counting technology indicated

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12

De Reys, S., C. Blom, B. Lepoudre, PJ Declerck, M. De Ley, J. Vermylen, and H. Deckmyn. "Human platelet aggregation by murine monoclonal antiplatelet antibodies is subtype-dependent." Blood 81, no. 7 (April 1, 1993): 1792–800. http://dx.doi.org/10.1182/blood.v81.7.1792.bloodjournal8171792.

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Twenty murine monoclonal antibodies (MoAbs) generated against different human platelet antigens induced clumping of human platelets in plasma and buffer. Whereas one MoAb could agglutinate platelets, clumping for 19 MoAbs was blocked by metabolic inhibitors, indicating that these induce platelet activation. Fifteen MoAbs were of IgG1, two of IgG2a, and two of IgG2b subtype. F(ab')2 fragments of these did not evoke an aggregatory response, but specifically inhibited aggregations by and binding of their respective intact MoAbs to platelets. Single-platelet counting technology indicated that the

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13

Simsek, S., and A. E. G. Kr von dem Borne. "Molecular Genetics of Human Platelet Antigens." Transfusion Medicine and Hemotherapy 21, no. 3 (1994): 29–33. http://dx.doi.org/10.1159/000223059.

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14

Kuijpers, RW, WH Ouwehand, PM Bleeker, D. Christie, and AE von dem Borne. "Localization of the platelet-specific HPA-2 (Ko) alloantigens on the N- terminal globular fragment of platelet glycoprotein Ib alpha." Blood 79, no. 1 (January 1, 1992): 283–88. http://dx.doi.org/10.1182/blood.v79.1.283.283.

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Abstract The human platelet-specific alloantigens HPA-2a and HPA-2b (= Kob and Koa) together constitute a biallelic antigen system. The HPA-2 antigens have not, to date, been located on a particular platelet membrane molecule. Here, we describe the localization of these antigens on platelet glycoprotein (GP) Ib alpha. Platelets from two patients with the Bernard-Soulier syndrome (BSS) were HPA-2(a-,b-) in the immunofluorescence test with HPA-2 alloantibodies on chloroquine- treated platelets. With monoclonal antibody (MoAb) immobilization of platelet antigen assay (MAIPA), positive reactions w

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15

Kuijpers, RW, WH Ouwehand, PM Bleeker, D. Christie, and AE von dem Borne. "Localization of the platelet-specific HPA-2 (Ko) alloantigens on the N- terminal globular fragment of platelet glycoprotein Ib alpha." Blood 79, no. 1 (January 1, 1992): 283–88. http://dx.doi.org/10.1182/blood.v79.1.283.bloodjournal791283.

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The human platelet-specific alloantigens HPA-2a and HPA-2b (= Kob and Koa) together constitute a biallelic antigen system. The HPA-2 antigens have not, to date, been located on a particular platelet membrane molecule. Here, we describe the localization of these antigens on platelet glycoprotein (GP) Ib alpha. Platelets from two patients with the Bernard-Soulier syndrome (BSS) were HPA-2(a-,b-) in the immunofluorescence test with HPA-2 alloantibodies on chloroquine- treated platelets. With monoclonal antibody (MoAb) immobilization of platelet antigen assay (MAIPA), positive reactions were obtai

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16

Scholz, Thomas, Uta Temmler, Siegfried Krause, Stan Heptinstall, and Wolfgang Lösche. "Transfer of Tissue Factor from Platelets to Monocytes: Role of Platelet-Derived Microvesicles and CD62P." Thrombosis and Haemostasis 88, no. 12 (2002): 1033–38. http://dx.doi.org/10.1055/s-0037-1613351.

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SummaryTissue factor (TF) is the most important initiator of intravascular coagulation. Platelets contribute to TF exposure on monocytes, but the mechanism is not completely understood. Here we examined the possibility that platelets may release TF that can be transferred to monocytes by platelet-derived microvesicles. When human citrated platelet-rich plasma was incubated with collagen there was an increase in the plasma levels of TF and CD62P. Incubation of plasma obtained from collagen-stimulated PRP with a sediment of red and white blood cells resulted in an increase in the number of monoc

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17

Fraser, JK, MF Leahy, and MV Berridge. "Expression of antigens of the platelet glycoprotein IIb/IIIa complex on human hematopoietic stem cells." Blood 68, no. 3 (September 1, 1986): 762–69. http://dx.doi.org/10.1182/blood.v68.3.762.762.

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Abstract Several cell surface and cytoplasmic markers specific for the megakaryocyte-platelet lineage have been described. However, as yet, none of these has been shown to be expressed on cells earlier than the committed megakaryocyte progenitor, CFU-Meg. The present study was aimed at determining whether platelet lineage antigens could be detected on human pluripotential stem cells. Rabbit antiserum against human platelets (APS) was extensively absorbed with erythrocytes and either platelets, neutrophils, monocytes, or cells of the monocytic cell line U937. The anti-stem cell antibodies in ea

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18

Fraser, JK, MF Leahy, and MV Berridge. "Expression of antigens of the platelet glycoprotein IIb/IIIa complex on human hematopoietic stem cells." Blood 68, no. 3 (September 1, 1986): 762–69. http://dx.doi.org/10.1182/blood.v68.3.762.bloodjournal683762.

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Several cell surface and cytoplasmic markers specific for the megakaryocyte-platelet lineage have been described. However, as yet, none of these has been shown to be expressed on cells earlier than the committed megakaryocyte progenitor, CFU-Meg. The present study was aimed at determining whether platelet lineage antigens could be detected on human pluripotential stem cells. Rabbit antiserum against human platelets (APS) was extensively absorbed with erythrocytes and either platelets, neutrophils, monocytes, or cells of the monocytic cell line U937. The anti-stem cell antibodies in each absorb

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19

Berridge, MV, SJ Ralph, and AS Tan. "Cell-lineage antigens of the stem cell-megakaryocyte-platelet lineage are associated with the platelet IIb-IIIa glycoprotein complex." Blood 66, no. 1 (July 1, 1985): 76–85. http://dx.doi.org/10.1182/blood.v66.1.76.76.

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Abstract The stem cell-platelet lineage is uniquely defined by platelet cell- lineage antigens. These antigens are present on all stem cells measured by the spleen colony assay and become restricted to the platelet cell lineage as differentiation proceeds. In this study, anti-platelet serum (APS) has been used to identify cells in the bone marrow that express platelet cell-lineage antigens and to identify platelet cell surface molecules expressing these antigens. Anti-platelet IgG extensively absorbed with brain, thymus, and peritoneal cells bound selectively to stem cells, megakaryocyte proge

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20

Berridge, MV, SJ Ralph, and AS Tan. "Cell-lineage antigens of the stem cell-megakaryocyte-platelet lineage are associated with the platelet IIb-IIIa glycoprotein complex." Blood 66, no. 1 (July 1, 1985): 76–85. http://dx.doi.org/10.1182/blood.v66.1.76.bloodjournal66176.

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The stem cell-platelet lineage is uniquely defined by platelet cell- lineage antigens. These antigens are present on all stem cells measured by the spleen colony assay and become restricted to the platelet cell lineage as differentiation proceeds. In this study, anti-platelet serum (APS) has been used to identify cells in the bone marrow that express platelet cell-lineage antigens and to identify platelet cell surface molecules expressing these antigens. Anti-platelet IgG extensively absorbed with brain, thymus, and peritoneal cells bound selectively to stem cells, megakaryocyte progenitor cel

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21

Lim, C., D. P. Manage, A. Atrazhev, G. Denomme, C. J. Backhouse, and J. P. Acker. "Microfluidic approach to genotyping human platelet antigens." IET Nanobiotechnology 6, no. 2 (2012): 33. http://dx.doi.org/10.1049/iet-nbt.2011.0044.

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22

Castro, Vagner. "Human platelet antigens and primary immune thrombocytopenia." Revista Brasileira de Hematologia e Hemoterapia 39, no. 2 (April 2017): 95–97. http://dx.doi.org/10.1016/j.bjhh.2017.02.008.

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23

SONE, Naoaki, Kazuyuki YAMAGUCHI, Masahiko SUZUKI, Mutumasa YANABU, Tetsuji SOGA, Shosaku NOMURA, Hirokazu NAGATA, Terutoshi KOKAWA, and Kojiro YASUNAGA. "Some Monoclonal Anti-human-platelet Antibodies Recognize Dog Platelets as Antigens." Japanese Journal of Thrombosis and Hemostasis 1, no. 6 (1990): 482–88. http://dx.doi.org/10.2491/jjsth.1.482.

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24

Garraud, Olivier, Fabrice Cognasse, and Pierre Moncharmont. "Immunological Features in the Process of Blood Platelet-Induced Alloimmunisation, with a Focus on Platelet Component Transfusion." Diseases 7, no. 1 (January 14, 2019): 7. http://dx.doi.org/10.3390/diseases7010007.

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Alloimmunisation to platelet antigens is not uncommon; a large number of females, having had pregnancies, developed antibodies to Human Leukocyte Antigen (HLA) moieties harboured on their foetuses’ cells (inherited from the father(s)) that may conflict with further pregnancies and transfused Platelet Components occasionally. This is possible since platelets constitutionally express HLA class I molecules (though in copy numbers that consistently differ among individuals). Platelets also express HPA moieties that are variants of naturally expressed adhesion and aggregation molecules; HPA differe

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25

STANLEY, R. G., J. R. NGAIZA, E. ATIENO, G. JELL, K. FRANCKLOW, C. L. JACKSON, H. PARRY, and M. J. DOENHOFF. "Immune-dependent thrombocytopaenia in mice infected with Schistosoma mansoni." Parasitology 126, no. 3 (March 2003): 225–29. http://dx.doi.org/10.1017/s0031182002002858.

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As has been shown previously, immunologically intact mice with patent Schistosoma mansoni infections has a significantly lower mean platelet number than intact uninfected mice (P<0·0001). However, platelet numbers in T-cell deprived mice with patent infections were not significantly different from those in uninfected T-cell deprived mice. Also, platelet counts in both the infected and uninfected T-cell deprived groups were not significantly different from those in intact uninfected mice. The S. mansoni-induced thrombocytopaenia in mice is thus seemingly immune dependent. Immunologically int

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26

Gruel, Y., B. Boizard, F. Daffos, F. Forestier, J. Caen, and JL Wautier. "Determination of platelet antigens and glycoproteins in the human fetus." Blood 68, no. 2 (August 1, 1986): 488–92. http://dx.doi.org/10.1182/blood.v68.2.488.bloodjournal682488.

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The autosomal recessive transmission of Glanzmann's thrombasthenia (GT) and Bernard-Soulier syndrome (BSS), together with requests of families who already had children with these diseases, prompted us to investigate the feasibility of their antenatal diagnosis. The preliminary step leading to the early detection of GT or BSS was to characterize, in the normal human fetus, the platelet antigens and glycoproteins (GPs) and to define their normal amounts on the membrane surface. Blood samples from 32 fetuses between 18 to 26 weeks of gestation were collected by direct puncture of the umbilical ve

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27

Ghevaert, Cedric, David A. Wilcox, Juan Fang, Kathryn Armour, Mike R. Clark, Willem H. Ouwehand, and Lorna M. Williamson. "Recombinant Human HPA-1A Antibodies for Treatment of Fetomaternal Alloimmune Thrombocytopenia (FMAIT): Proof of Principle in An in Vivo Murine Model and Human Volunteer Studies." Blood 112, no. 11 (November 16, 2008): 85. http://dx.doi.org/10.1182/blood.v112.11.85.85.

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Abstract Fetomaternal alloimmune thrombocytopenia (FMAIT) is caused by maternal generation of antibodies specific for paternal platelet antigens and can lead to fetal intracranial hemorrhage. A single nucleotide polymorphism (SNP) in the gene encoding integrin β3 causes a clinically important maternal-paternal antigenic difference; Leu33 generates the human platelet antigen 1a (HPA-1a), whereas Pro33 generates HPA-1b. As a potential treatment to prevent fetal intracranial hemorrhage in HPA-1a alloimmunized pregnancies, we generated an antibody that blocks the binding of maternal HPA-1a–specifi

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28

Gruel, Y., B. Boizard, F. Daffos, F. Forestier, J. Caen, and JL Wautier. "Determination of platelet antigens and glycoproteins in the human fetus." Blood 68, no. 2 (August 1, 1986): 488–92. http://dx.doi.org/10.1182/blood.v68.2.488.488.

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Abstract The autosomal recessive transmission of Glanzmann's thrombasthenia (GT) and Bernard-Soulier syndrome (BSS), together with requests of families who already had children with these diseases, prompted us to investigate the feasibility of their antenatal diagnosis. The preliminary step leading to the early detection of GT or BSS was to characterize, in the normal human fetus, the platelet antigens and glycoproteins (GPs) and to define their normal amounts on the membrane surface. Blood samples from 32 fetuses between 18 to 26 weeks of gestation were collected by direct puncture of the umb

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29

Kunicki, TJ, R. Orchekowski, D. Annis, and Y. Honda. "Variability of integrin alpha 2 beta 1 activity on human platelets." Blood 82, no. 9 (November 1, 1993): 2693–703. http://dx.doi.org/10.1182/blood.v82.9.2693.2693.

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Abstract The activity and surface antigenicity of alpha 2 beta 1 on platelets from 27 normal subjects were found to vary significantly. A fourfold range of surface antigen correlates with a 20-fold variation in the ability of nonactivated, washed platelets to adhere to type I collagen and a fivefold variation in the adhesion of platelets to type III collagen. These differences in surface receptor are reflected in significant variation in the lag time required for type I collagen- induced platelet aggregation in platelet-rich plasma. Among the same individuals, no difference was observed in sur

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30

Kunicki, TJ, R. Orchekowski, D. Annis, and Y. Honda. "Variability of integrin alpha 2 beta 1 activity on human platelets." Blood 82, no. 9 (November 1, 1993): 2693–703. http://dx.doi.org/10.1182/blood.v82.9.2693.bloodjournal8292693.

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The activity and surface antigenicity of alpha 2 beta 1 on platelets from 27 normal subjects were found to vary significantly. A fourfold range of surface antigen correlates with a 20-fold variation in the ability of nonactivated, washed platelets to adhere to type I collagen and a fivefold variation in the adhesion of platelets to type III collagen. These differences in surface receptor are reflected in significant variation in the lag time required for type I collagen- induced platelet aggregation in platelet-rich plasma. Among the same individuals, no difference was observed in surface leve

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31

Bertrand, Gérald, Vincent Jallu, Maxime Gouet, Killie Mette Kjaer, Patrick Lambin, Anne Husebekk, and Cécile Kaplan. "Quantification of human platelet antigen-1a antibodies with the monoclonal antibody immobilization of platelet antigens procedure." Transfusion 45, no. 8 (June 10, 2005): 1319–23. http://dx.doi.org/10.1111/j.1537-2995.2005.00195.x.

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32

Hutchinson, Tyler Davi d., Yuhua Song, Kevin Trainor, and Ghazala Hashmi. "Disequilibrium of Human Platelet Antigen 1 (HPA-1) in U.S. Population." Blood 112, no. 11 (November 16, 2008): 5466. http://dx.doi.org/10.1182/blood.v112.11.5466.5466.

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Abstract Background: Alloimmunization against Human Platelet Antigens (HPA) is associated with Neonatal Alloimmune Thrombocytopenia (NAIT), post-transfusion purpura and refractoriness for platelet transfusion. A flexible BeadChip™ design was developed to simultaneously detect 22 platelet antigens, including HPA-1, and used to assay over 1,000 random blood donors from across the United States. Methods: Samples from 19 labs/centers from across the country were assayed for 11 HPA loci (HPA-1 through 9, 11 and 15) using the BioArray Solutions HPA Assay. Each locus was independently assessed for Ha

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33

Choi, ES, JL Nichol, MM Hokom, AC Hornkohl, and P. Hunt. "Platelets generated in vitro from proplatelet-displaying human megakaryocytes are functional." Blood 85, no. 2 (January 15, 1995): 402–13. http://dx.doi.org/10.1182/blood.v85.2.402.bloodjournal852402.

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An in vitro culture system demonstrating the transitions from megakaryocyte progenitors to functional platelets is described. CD34- selected cells from normal human peripheral blood are cultured under conditions that promote megakaryocyte formation. After 8 to 11 days, enriched populations of mature megakaryocytes are replated under conditions that favor the development of proplatelets. Proplatelets express the platelet-specific proteins, glycoproteins Ib and IIb (GPIb and GPIIb), and fibrinogen and also contain microtubule coils equal in size to those found in plasma-derived platelets. In add

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34

Rock, Gail, and Maria Kolajova. "Proteomics Used To Identify the Target of a Platelet Aggregating Antibody in a Patient with HUS." Blood 104, no. 11 (November 16, 2004): 852. http://dx.doi.org/10.1182/blood.v104.11.852.852.

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Abstract Hemolytic Uremic Syndrome (HUS) has considerable overlap with Thrombotic Thrombocytopenia Purpura (TTP). Recently, evidence is emerging to suggest that TTP, like HIT, is an immune mediated disorder. We have investigated the plasmas of patients with Hemolytic Uremic Syndrome to determine the presence of antibodies and the specificity of the related antigens. Methods: A 20 year old female presented with repeated episodes of HUS. She is dialysis dependent. Plasma was taken for VWF, multimers, platelet aggregation, metalloprotease and inhibitor, western blot and 2D PAGE analysis. Results:

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35

Gilson, Christopher R., Seema R. Patel, and James C. Zimring. "Co-Stimulatory Blockade Abrogates Alloimmunization to Transfused Platelets in a Mouse Model." Blood 118, no. 21 (November 18, 2011): 717. http://dx.doi.org/10.1182/blood.v118.21.717.717.

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Abstract Abstract 717 Background: Platelet transfusion therapy can be a life-sustaining treatment for patients with severe thrombocytopenia. However, alloimmunization is a potential sequelae of platelet transfusion with serious consequences for chronically transfused patients. Induction of alloantibodies, typically against HLA and/or human platelet antigens, can lead to poor survival of transfused platelets expressing the offending antigens. Patients with alloantibodies against multiple HLAs can become refractory to subsequent platelet therapy. Although leukoreduction of platelets has signific

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36

Fischer, T. H., D. W. Barton, K. H. Krause, T. E. White, K. P. Campbell, and G. C. White. "The identification of sarcoplasmic reticulum terminal cisternae proteins in platelets." Biochemical Journal 263, no. 2 (October 15, 1989): 605–8. http://dx.doi.org/10.1042/bj2630605.

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Two new proteins with apparent molecular masses of 53 kDa and 190 kDa have been identified in both sarcoplasmic reticulum and human blood platelets using a monoclonal antibody, FII1b5. The sarcoplasmic reticulum FII1b5 antigens were present in the terminal cisternae fraction, but were absent from light sarcoplasmic reticulum. The platelet and skeletal muscle proteins were not sensitive to digestion with endoglycosidase H under conditions that removed carbohydrate from the 53 kDa glycoprotein in sarcoplasmic reticulum or GPIIIa in platelet microsomes and did not bind 45Ca in a nitrocellulose ov

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37

Bachelot, Christilla, Raphaël Saffroy, Sophie Gandrille, Martine Aiach та Francine Rendu. "Role of FCγRIIA Gene Polymorphism in Human Platelet Activation by Monoclonal Antibodies". Thrombosis and Haemostasis 74, № 06 (1995): 1557–63. http://dx.doi.org/10.1055/s-0038-1649982.

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SummaryThe aim of this study was to determine if there is a correlation between the activity of a MoAb as an agonist and its ability to bind to the Fc platelet receptor, FcγRIIa. A polymorphism at amino acid 131 [arginine (Arg) or histidine (His)] of FcγRIIa was first shown to be determinant for MoAb-IgG1 binding on monocytes. To clarify the role of this polymorphism in platelet activation by MoAb-IgG1 we (i) established the FCγRIIA polymorphism at the gene level by adapting the denaturating gradient gel electrophoresis method, (ii) analyzed the binding affinity of the MoAbs to FrγRIIa on plat

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38

Stenziger, Werner, Beate Kehrel, and Jürgen van de Loo. "Identification of Platelet Antigens by Immunoprecipitation of Unlabelled Platelet Glycoproteins." Thrombosis and Haemostasis 64, no. 03 (1990): 469–72. http://dx.doi.org/10.1055/s-0038-1647338.

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SummaryA time-saving and sensitive method for the identification of antigens on unlabelled platelet glycoproteins (GP) based on immunoprecipitation has been developed. Platelet solubilisates were incubated with antibodies to form GP-antibody complexes that were precipitated with Protein G Sepharose 4 Fast Flow (PGS). Pcs-bound material was eluted, separated by SDSPAGE under reducing conditions and visualized by silver staining. The method was designed as an alternative to radioimmunoprecipitation for laboratories not equipped to work with radioactive substances. It is proposed as a complementa

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Choi, ES, JL Nichol, MM Hokom, AC Hornkohl, and P. Hunt. "Platelets generated in vitro from proplatelet-displaying human megakaryocytes are functional." Blood 85, no. 2 (January 15, 1995): 402–13. http://dx.doi.org/10.1182/blood.v85.2.402.402.

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Abstract An in vitro culture system demonstrating the transitions from megakaryocyte progenitors to functional platelets is described. CD34- selected cells from normal human peripheral blood are cultured under conditions that promote megakaryocyte formation. After 8 to 11 days, enriched populations of mature megakaryocytes are replated under conditions that favor the development of proplatelets. Proplatelets express the platelet-specific proteins, glycoproteins Ib and IIb (GPIb and GPIIb), and fibrinogen and also contain microtubule coils equal in size to those found in plasma-derived platelet

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Chang, Y. W., J. Mytilineos, G. Opelz, and B. R. Hawkins. "Distribution of human platelet antigens in a Chinese population." Tissue Antigens 51, no. 4 (September 30, 2008): 391–93. http://dx.doi.org/10.1111/j.1399-0039.1998.tb02979.x.

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Platt, Jeffrey L., and Zoie E. Holzknecht. "PORCINE PLATELET ANTIGENS RECOGNIZED BY HUMAN XENOREACTIVE NATURAL ANTIBODIES." Transplantation 57, no. 3 (February 1994): 327–35. http://dx.doi.org/10.1097/00007890-199402150-00003.

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De La Vega Elena, C. D., N. Nogués, A. Fernández Montoya, S. Chialina, P. D. Blanzaco, E. Theiller, M. A. Raillon, et al. "Human platelet-specific antigens frequencies in the Argentinean population." Transfusion Medicine 18, no. 2 (April 2008): 83–90. http://dx.doi.org/10.1111/j.1365-3148.2007.00819.x.

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Vazmitsel, Maryna, Dong Chen, Barbara Gruner, and Emily Coberly. "An Unusual Case of Fetal/Neonatal Alloimmune Thrombocytopenia." American Journal of Clinical Pathology 152, Supplement_1 (September 11, 2019): S151—S152. http://dx.doi.org/10.1093/ajcp/aqz131.002.

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Abstract Objectives Fetal/neonatal alloimmune thrombocytopenia (FNAIT) occurs when maternal IgG alloantibodies against paternal human platelet antigens (HPA) cross the placenta and cause the destruction of fetal platelets. The vast majority (up to 95%) of FNAIT cases are caused by antibodies against HPA-1a or HPA-5b antigens, while the remaining cases are usually due to antibodies against a variety of other HPA antigens. Cases of FNAIT due to anti-HLA antibodies are extremely uncommon and have only rarely been reported. We present a case of FNAIT suspected to be caused by anti-HLA class I allo

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Rathore, Vipul, Matthew Meyers, and Bryan Ray. "PAKTM-Lx: A New Luminex*®-Based Assay to Detect and Identify Antibodies to Human Platelet Antigens (HPA) in Patient Serum." Blood 114, no. 22 (November 20, 2009): 4187. http://dx.doi.org/10.1182/blood.v114.22.4187.4187.

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Abstract Abstract 4187 Platelets express a variety of glycoproteins (GPIIb-IIIa, GPIa-IIa, GPIb/IX, GPIV, CD109 and Class I HLA). Human Platelet Antigens (HPA) represent polymorphisms of these platelet surface glycoproteins. While these polymorphisms do not alter the function of the proteins, they can become target of the immune system in mismatched individuals. Alloantibodies against HPA are involved in the pathogenesis of Neonatal Allo-Immune Thrombocytopenia (NAIT), Post-Transfusion Purpura (PTP) and refractoriness to random donor platelets. In addition to generating anti-HPA antibodies, th

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Lin, Xin, Ermelina Enriquez, Jigar Patel, Ruth Huang, Cindi Marks, Sunitha Vege, KL Billingsley, Joann M. Moulds, and Ghazala Hashmi. "Universal DNA Arrays for High-Throughput SNP Detection of Human Platelet Antigens (HPA)." Blood 116, no. 21 (November 19, 2010): 4403. http://dx.doi.org/10.1182/blood.v116.21.4403.4403.

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Abstract Abstract 4403 Background: DNA analysis of human platelet antigens is known to improve the diagnosis and treatment of neonatal alloimmune thrombocytopenia and minimize the risks of post transfusion purpura and refractoriness to random donor platelet therapy. The availability of reliable molecular platforms such as HPA eMAP assays analyzing HPA-1, -2, -3, -4, -5, -6, -7, -8, -9, -11, and -15, are routinely used and eliminate the need for reference sera or large platelet volumes. New generations of HPA assays (HPA eMAP-S Beadchip™ Kit) described here are developed by identification of sp

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Simsek, S., NM Faber, PM Bleeker, AB Vlekke, E. Huiskes, R. Goldschmeding, and AE von dem Borne. "Determination of human platelet antigen frequencies in the Dutch population by immunophenotyping and DNA (allele-specific restriction enzyme) analysis." Blood 81, no. 3 (February 1, 1993): 835–40. http://dx.doi.org/10.1182/blood.v81.3.835.835.

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Abstract Platelets from 200 random Dutch blood donors were typed for the human platelet alloantigens HPA-1 to -5 recognized at present and for Naka. Naka is an epitope on glycoprotein IV, not expressed on the platelet of individuals with hereditary GP IV deficiency. Platelet immunofluorescence and monoclonal antibody-specific immobilization of platelet antigens (MAIPA) were applied for this purpose. The observed phenotype frequencies were 97.86% and 28.64% for HPA-1a and -1b, 100% and 13.15% for HPA-2a and -2b, 80.95% and 69.84% for HPA-3a and -3b, 100% and 0% for HPA-4a and -4b, 100% and 19.7

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47

Simsek, S., NM Faber, PM Bleeker, AB Vlekke, E. Huiskes, R. Goldschmeding, and AE von dem Borne. "Determination of human platelet antigen frequencies in the Dutch population by immunophenotyping and DNA (allele-specific restriction enzyme) analysis." Blood 81, no. 3 (February 1, 1993): 835–40. http://dx.doi.org/10.1182/blood.v81.3.835.bloodjournal813835.

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Platelets from 200 random Dutch blood donors were typed for the human platelet alloantigens HPA-1 to -5 recognized at present and for Naka. Naka is an epitope on glycoprotein IV, not expressed on the platelet of individuals with hereditary GP IV deficiency. Platelet immunofluorescence and monoclonal antibody-specific immobilization of platelet antigens (MAIPA) were applied for this purpose. The observed phenotype frequencies were 97.86% and 28.64% for HPA-1a and -1b, 100% and 13.15% for HPA-2a and -2b, 80.95% and 69.84% for HPA-3a and -3b, 100% and 0% for HPA-4a and -4b, 100% and 19.7% for HPA

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Roz̆man, Primoz̆. "Platelet antigens. The role of human platelet alloantigens (HPA) in blood transfusion and transplantation." Transplant Immunology 10, no. 2-3 (August 2002): 165–81. http://dx.doi.org/10.1016/s0966-3274(02)00063-1.

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Vassallo, Ralph R. "Recognition and management of antibodies to human platelet antigens in platelet transfusion-refractory patients." Immunohematology 25, no. 3 (2020): 119–24. http://dx.doi.org/10.21307/immunohematology-2019-244.

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Franceschi, F., R. M. Genta, A. Gasbarrini, E. C. Nista, A. R. Sepulveda, R. De Cristofaro, R. Tartaglione, et al. "Cross-reactivity between anti-CagA antibodies and human platelet antigens." Digestive and Liver Disease 32 (November 2000): A85. http://dx.doi.org/10.1016/s1590-8658(00)80517-4.

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