Relevant bibliographies by topics / Human platelet antigens

Academic literature on the topic 'Human platelet antigens'

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Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Human platelet antigens"

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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 +/- 20,016 (mean +/- SD); its range was between 54,782 to 116,185 molecules per platelet. After treatment with chloroquine, 79.9 +/- 7.0% (mean +/- SD, n = 6) of HLA antigens were removed from platelets as determined by binding of 125I-W6/32 Fab. A similar result was obtained when HLA antigens on chloroquine-treated platelets were evaluated with immunofluorescence flow cytometry. In contrast, chloroquine treatment did not remove integral membrane protein such as P1A1 antigens on platelets. The presence of HLA antigens in the chloroquine eluate of platelets could be demonstrated to contain HLA antigens similar in mol wts to intact class I molecules by an immunoblotting technique. These data suggest that 70% to 80% of platelet HLA antigens are adsorbed and that such HLA antigens are not proteolytic products of integral membrane class I molecules. The origin of the adsorbed platelet HLA-antigens remains to be determined.
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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 (mean +/- SD); its range was between 54,782 to 116,185 molecules per platelet. After treatment with chloroquine, 79.9 +/- 7.0% (mean +/- SD, n = 6) of HLA antigens were removed from platelets as determined by binding of 125I-W6/32 Fab. A similar result was obtained when HLA antigens on chloroquine-treated platelets were evaluated with immunofluorescence flow cytometry. In contrast, chloroquine treatment did not remove integral membrane protein such as P1A1 antigens on platelets. The presence of HLA antigens in the chloroquine eluate of platelets could be demonstrated to contain HLA antigens similar in mol wts to intact class I molecules by an immunoblotting technique. These data suggest that 70% to 80% of platelet HLA antigens are adsorbed and that such HLA antigens are not proteolytic products of integral membrane class I molecules. The origin of the adsorbed platelet HLA-antigens remains to be determined.
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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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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 cell (RBC) phenotype. Among A1 donors, platelet ABH varied significantly between donors (0%-87%). Intradonor variability, however, was minimal, suggesting that platelet ABH expression is a stable, donor-specific characteristic, with 5% of A1 donors typing as either ABH high- or low-expressers. Group A2 donors, in contrast, possessed a Bombay-like phenotype, lacking both A and H antigens. Unlike RBCs, ABH expression on platelets may be determined primarily by H-glycosyltransferase (FUT1) activity. Identification of A2 and A1 low expressers may increase the availability and selection of crossmatched and HLA-matched platelets. Platelets from group A2 may also be a superior product for patients undergoing A/O major mismatch allogeneic progenitor cell transplantation. (Blood. 2005;105:3356-3364)
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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 effects on antigen-specific CD8+ T cells in sepsis in vivo and ex vivo. We discovered that both human and murine platelets internalize and proteolyze exogenous antigens, generating peptides that are loaded onto MHC-I. The expression of platelet MHC-I, but not platelet MHC-II, is significantly increased in human and murine platelets during sepsis and in human megakaryocytes stimulated with agonists generated systemically during sepsis (eg, interferon-γ and lipopolysaccharide). Upregulation of platelet MHC-I during sepsis increases antigen cross-presentation and interactions with CD8+ T cells in an antigen-specific manner. Using a platelet lineage–specific MHC-I–deficient mouse strain (B2Mf/f-Pf4Cre), we demonstrate that platelet MHC-I regulates antigen-specific CD8+ T-cell proliferation in vitro, as well as the number and functional responses of CD8+ T cells in vivo, during sepsis. Loss of platelet MHC-I reduces sepsis-associated mortality in mice in an antigen-specific setting. These data identify a new mechanism by which platelets, through MHC-I, process and cross-present antigens, engage antigen-specific CD8+ T cells, and regulate CD8+ T-cell numbers, functional responses, and outcomes during sepsis.
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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. Fibrinogen was also localized to the osteoclast membrane in foetal bone imprints. In addition, we found that CD9 and gpIIIa antibodies reacted weakly with monocytes in buffy coat smears. Antibodies to factor 8 and glycoproteins Ib and IIb/IIIa did not react with osteoclasts. These results show that osteoclasts, monocytes, macrophages, megakaryocytes and platelets possess common antigens and that fibrinogen is present on the surface of osteoclasts. By analogy with platelets, CD9 and gpIIIa may play a role in fibrinogen binding by osteoclasts. Possible mechanisms by which platelet antigens and fibrinogen binding could affect osteoclast function are proposed.
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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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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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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+ and Ia-; all other lymphocyte and platelet antigens were not detected. (b) Myeloid cells at all stages of differentiation (promyelocytes, myelocytes, metamyelocytes, and neutrophils) were HLA-ABC+; beta 2m+; HuLy-m1-, m2-, m3+/- (20%), m4+, m5+/- (20%); HuPl-m1-; in addition, promyelocytes and myelocytes were Ia+ but neutrophils and metamyelocytes were Ia-. (c) Lymphocytes were HLA-ABC+, beta 2m+, Ia+/- (20-30%), HuLy-m1+/- (40-50%), m2+/- (60-70%), m3+, m4+, m5+; Pl-m1-. (d) Platelets and megakaryocytes were HLA-ABC+; beta 2m+; Ia-; HuLy-m1+-, m2-, m3-, m4-, m5-, HuPl-m1+, and the putative "megakaryocyte precursors" were HuPl-m1+, Ia-, HuLy-m1-. The different cell types in bone marrow could readily be distinguished, particularly cells of the myeloid series (Ia and HuLy-m4, m5), lymphocytes (Ia and HuLy-m1, m2, m3), and platelets and their precursor cells (HuPl-m1). This simple method of defining cellular phenotypes in bone marrow has demonstrated the practicality of using monoclonal antibodies to identify marrow cells and should be of diagnostic value.
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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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Dissertations / Theses on the topic "Human platelet antigens"

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Bouwmans, Eva Lamberta Antonia. "Human platelet antigen-1a presentation and antibody generation." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610311.

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De, Leon Ellen Jane Biotechnology &amp Biomolecular Sciences Faculty of Science UNSW. "Engineering antibodies against complex platelet antigens using phage display technology." Awarded by:University of New South Wales, 2007. http://handle.unsw.edu.au/1959.4/37009.

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Platelets are small anucleate cell fragments found in blood whose physiological role is important in maintaining haemostasis. In vivo, platelet surface glycoproteins mediate the mechanistic roles of platelets, and polymorphic changes to these glycoproteins have been observed to have significant effects on the platelet cellular function and such changes may include over-expression, under-expression and antigenicity of the protein. Human platelet antigens (HPA) are a result of polymorphic differences in platelet surface glycoproteins which have been found to be variably expressed in the population. Foetal maternal alloimmune thrombocytopaenia (FMAIT) is a condition that is observed in the unborn foetus and neonates due to HPA incompatibility between the mother and the foetus. HPA incompatibility accounts for a majority of severe thrombocytopaenic cases in neonates, and delayed diagnosis and treatment of such a condition often lead to intracranial haemorrhage. The risk in neonates diagnosed with FMAIT becomes increasingly significant in cases where intra-uterine (during pregnancy) platelet transfusion is the only effective therapeutic option. There are currently no antenatal screening programs for this condition, and laboratory diagnosis of FMAIT relies on the detection of maternal alloantibodies and parental HPA typing. For these reasons a significant amount of research is currently being invested into the isolation of recombinant antibodies with specific reactivity against FMAIT-related platelet antigens. Stable and specific recombinant platelet antibodies have great potential as a diagnostic agent in antenatal screening and broad-scale HPA typing of blood donors for platelet transfusion. Further characterisation of the isolated antibody may lead to a possible therapeutic agent. Studies by previous researchers have shown that the traditional methods (ie. Mouse monoclonal and EBV transformation) of obtaining monoclonal antibodies against FMAIT-related antigens have proven unsuccessful. The continuing progress in the discipline of phage display has produced several novel antibodies against self and non-self antigens. A further advantage in the application of phage display technology for the isolation of novel antibodies is the easy transition from bacterial to mammalian expression for the characterisation of glycosylated antibodies. The main focus of this project was to create and isolate a recombinant human anti-HPA-3a antibody using phage display for its possible application as a therapeutic or diagnostic agent.
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Pilebro, Lappalainen Ida. "A new quick method for screening of HPA-1 based on fluorescence conjugated antibodies." Thesis, Uppsala universitet, Institutionen för kvinnors och barns hälsa, 2018. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-356042.

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Human platelet antigens (HPA) is located on the platelet surface and they are inherited both from the mother and the father. If a mother who is homozygous for HPA-1b carries a child who has inherited HPA-1a from the father, the mother is in danger to form antibodies against HPA-1a on the fetal platelet. This may cause the child to suffer from neonatal alloimmune thrombocytopenia (NAIT) that could lead to death. This can be prevented by platelet transfusion. EVA Biosensor Technology is a new method for detection of HPA-1 that is currently only approved for scientific research. The aim of this study was to evaluate EVAreader R6 and find HPA-1a negative platelet donors that can donate platelets to children born with NAIT. The test material consisted of blood samples from 513 male blood donors with blood group 0. The blood was lysed and tested in EVA-reader R6 from Davos Diagnostics. The result was shown on the screen after 10 min. The results that came out negative or intermediate was analyzed a second time. In total, nine HPA-1a negative donors and 503 HPA-1a positive donors were found. Approximately 2 % of the population is HPA-1a negative, which was reflected in the result. To make sure that the results are correct, a validation with an already existing method has to be made. The conclusion is that the EVA Biosensor Technology could be used for typing of HPA in the future, as long as the results from the validation is correct.
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Anani, Sarab Gholamreza. "Construction, expression and antigenic characterisation of recombinant human platelet antigen-1 (HPA-1)." Thesis, University of Aberdeen, 2010. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=158493.

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Previously it has been shown that sequences containing both Trp25 and Leu33 are the most effective at inducing Th cell proliferation in HLA-DRB3*0101 positive women, alloimmunised with anti-HPA-1a.  The Leu33/Pro33 polymorphism is embedded in the N-terminal plexin/semaphorin/integrin (PSI) domain of GPIIIa.  In the present study, amino acids 1-62 of the GPIIIa (Leu33 or Pro33) PSI domain were cloned into the vector pGEX-6p-1.  The recombinant proteins were expressed and tested by ELISA, Luminex and Absorption Assays.  The presence of the HPA-1a/-1b epitope was confirmed by the ability of PSI-Leu33/-Pro33 recombinant fragments to specifically capture its corresponding HPA-1 antibody.  Cells from a human B cell line (HHKB), homozygous for HLA-DRB3*0101, were pulsed with the recombinant PSI domain fragment of GPIIIa expressing the HPA-1a antigen.  MHC class II/peptide complexes were isolated from the pulsed cells using an immunoaffinity column.  A nested set of naturally processed and presented HPA-1a derived peptides, each containing the residues Trp25 – Leu33 core epitope was identified.  For the first time a naturally processed and presented HPA-1a peptide that spans the HPA-1a polymorphism has been identified, bound to the class II molecule encoded by HLA-DRB3*0101.  The efficient processing and presentation of this peptide, which includes the putative dominant Th epitope, is likely to be an important contributory factor in the immunogenicity of HPA-1a.  Such peptides may also provide the basis for novel treatments to tolerise the corresponding Th response in HPA-1b1b women at risk of NAIT with an HPA-1a-positive fetus.
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Allen, David L. "A study of the Human Platelet Antigen 1a (HPA-1a) antibody response in neonatal alloimmune thrombocytopenia (NAIT)." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:44a10539-de5d-44dc-9c51-5f43cf3c3a82.

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Neonatal alloimmune thrombocytopenia (NAIT) is caused by maternal alloantibodies against fetal platelet antigens inherited from the father and which are absent from maternal platelets. In Caucasians, antibodies against the Leu33 (HPA-1a) polymorphism of integrin β3 (part of the platelet αIIbβ3 complex) account for >70% of cases. Antenatal screening for these antibodies does not currently take place in the UK, partly because of the absence of sensitive, predictive tests. We hypothesized that the poor sensitivity and predictive abilities of current assays are due to the use of β3 in an inappropriate conformation, resulting in sub-optimal binding of HPA-1a antibodies. We hypothesized firstly that in vitro induced changes to αIIbβ3 might alter accessibility of the HPA-1a epitopes to alloantibodies, thus reducing assay sensitivity. Secondly, we hypothesized that HPA-1a antibodies are stimulated by, and preferentially recognise, β3 in association with αv, a molecule present on placental syncytiotrophoblasts, and that reactivity against platelet αIIbβ3 reflects only cross-reactivity with αvβ3. Our first hypothesis was proven by demonstrating that use of the cation chelating compound EDTA, used by many diagnostic laboratories as a component of assay reagents or present in blood samples as anticoagulant, resulted in significantly reduced assay sensitivity. These findings were confirmed in an international workshop. Support for our second hypothesis was provided by demonstrating enhanced reactivity of a small panel of examples of anti-HPA-1a against αvβ3 compared to αIIbβ3 and by molecular modelling data. We also showed that HPA-1a antibodies can inhibit platelet function by using a novel application of the ROTEM® delta thromboelastograph and an immunofluorescence assay in which we demonstrated blocking of platelet function using a monoclonal antibody, PAC-1, that binds only to activated αIIbβ3. These studies provide possible explanations for the poor sensitivity and predictive abilities of current assays and suggest further areas for research.
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Jennings, Brent. "Comparison between endocytosis and intracanalicular sequestration of cell-surface antigens in human platelets." Master's thesis, University of Cape Town, 1992. http://hdl.handle.net/11427/26566.

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Human platelets respond to various macromolecules in the plasma. Uptake of specific ligands, and antibodies to various epitopes on the platelet plasma membrane, has been observed. The platelet canalicular system has been shown to be involved with this uptake. Recently, investigators have speculated on the role of endocytosis in platelets to account for the presence of plasma proteins such as fibrinogen and immunoglobulin within platelet organelles. Antibodies binding to cell-surface antigens on platelets can lead to a redistribution of these antigens. When antibodies, specific for platelet cell-surface receptors, bind to platelets they may either undergo endocytosis into intracellular vacuoles, or may merely become sequestered within the canalicular system of platelets. The present study investigated whether endocytosis occurs in platelets. Such a process would lead to the endocytic uptake of a fluid-phase marker and would involve internalization and recycling of cell surface membrane. A fluid-phase marker (FITC-dextran) was used to measure any constitutive endocytic activity. In addition, a suitable membrane marker was used to determine whether membrane internalization occurred. This involved a technique whereby radioactive galactose was covalently attached to cell-surface glycoconjugates. A monoclonal antibody to the platelet receptor, GPIIbIIIa, was used in conjunction with the membrane marker in order to determine if membrane internalization was involved during the subsequent redistribution of the receptor-antibody complex. Immunocytochemical techniques using electron-dense probes were employed to localise the sites to which this receptor-antibody complex became redistributed. In comparison with reported rates of endocytic uptake of fluid-phase marker in other cell types, no significant endocytic activity could be detected with platelets, after taking their relatively small volume into account. Similarly, membrane internalization was not detected with resting platelets. Following challenge of the platelets with anti-GPIIbIIIa antibody, no membrane internalization could be measured during redistribution of the receptor-antibody complex. The compartment to which the receptor-antibody complex was redistributed could be identified morphologically as the canalicular system. The present data provide evidence for a process of sequestration of receptor-antibody in the canalicular system of resting platelets. It remains possible that other mechanisms exist within the platelet system for uptake of extracellular material as this study dealt exclusively with the platelet response to a specific antibody. These results may have implications with respect to the interaction of platelets with anti-platelet antibodies in the normal state, as well as with clinical disorders involving elevated levels of platelet-associated IgG. As far as can be deduced from the available literature, these data represent the first use of a covalent membrane marker in conjunction with uptake of macromolecules to study endocytic events in human platelets.
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Neudert, Christiane. "Untersuchungen zum Einfluss von Human-Platelet-Antigen-1b (HPA-1b), Faktor-V-Mutation (G1691A, Faktor V-Leiden), Prothrombin-Mutation (G20210A) und Methylentetrahydrofolat-Reduktase-Polymorphismus (MTHFR 677TT) auf den postoperativen Verlauf nach aortokoronarer Bypass-Operation." [S.l.] : [s.n.], 2000. http://deposit.ddb.de/cgi-bin/dokserv?idn=96200121X.

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Foxcroft, Zyta Krystyna. "Human platelet antigen frequencies in the South African blood donor population determined by polymerase chain reaction with sequence-specific primers." Thesis, 2008. http://hdl.handle.net/10210/439.

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Platelets play an integral part in the blood clotting process. The normal platelet count ranges from 150 to 400 x 103/μl. To date, twenty-four platelet-specific antigens have been defined. Human Platelet Antigens (HPA) 1-5 and –15 belong to diallelic systems and antibodies formed in response to immunization against these antigens, following transfusion or transplacental haemorrhage, have been responsible for life-threatening conditions in which the platelet counts of patients are markedly decreased. This is due to the destruction of platelets by platelet antigen - specific antibodies in Neonatal Alloimmune Thrombocytopenia and Post-Transfusion Purpura and in some instances, Platelet Refractoriness. In these clinical situations, transfusions of platelets from random donors do not result in post-transfusion platelet increments. Ideally, a database of blood donors who have been HPA typed should be established. This database can then be used to search for HPA – compatible donors and matched platelet donations can be made available to these patients. The aims of this study were primarily to determine the HPA frequencies in the South African blood donor population and establish a register of HPA-typed donors. Secondly, the established frequencies would be compared to those of other world populations. Anticoagulated blood samples from one hundred and fifty donors from each of the four main South African population groups were obtained for typing of HPA 1-5 and –15 by the PCR-SSP method in order to determine their gene and genotype frequencies and establish a platelet donor database. Two methods of analyses were used to determine statistical similarities and differences between the South African population and a number of world populations (X2) and the degree of genetic distance between them (FST). Phylogenetic trees and Principal Components plots were constructed to illustrate relationships between populations. The HPA gene and genotype frequencies of the South African blood donor population have been determined. An accurate, rapid method of HPA typing has been validated and effective HPA matched platelet transfusions are now possible for the first time in South Africa. The gene frequencies of the White population have been found to be similar to those from European populations and the Bantu-speaking population frequencies compared favourably with those of other African populations. The population group of mixed ethnicity (Coloured) was shown to have unique frequencies and were not similar to any of those populations chosen for comparison except with the other populations in South Africa.
Dr. R. L. Crookes Prof. T.L. Coetzer Prof. M. Dutton
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Jacobs, Collin [Verfasser]. "Der "human platelet antigen-1" (HPA-1)-Polymorphismus beeinflusst nicht die Wirkungen von Glykoprotein-IIb-IIIa-Inhibitoren / vorgelegt von Collin Jacobs." 2005. http://d-nb.info/979565359/34.

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Roberts, Wayne, S. Magwenzi, Ahmed Aburima, and Khalid M. Naseem. "Thrombospondin-1 induces platelet activation through CD36-dependent inhibition of the cAMP/protein kinase A signaling cascade." 2010. http://hdl.handle.net/10454/6155.

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Cyclic adenosine monophosphate (cAMP)-dependent signaling modulates platelet function at sites of vascular injury. Here we show that thrombospondin-1 (TSP-1) prevents cAMP/protein kinase A (PKA) signaling through a CD36-dependent mechanism. Prostaglandin E(1) (PGE(1)) induced a robust inhibition of both platelet aggregation and platelet arrest under physiologic conditions of flow. Exogenous TSP-1 reduced significantly PGE(1)-mediated inhibition of both platelet aggregation and platelet arrest. TSP-1 prevented PGE(1)-stimulated cAMP accrual and phosphorylation of PKA substrates, through a mechanism requiring phosphodiesterase3A. TSP-1 also inhibited VASP phosphorylation stimulated by the nonhydrolyzable cAMP analog, 8-bromo-cAMP, indicating that it may regulate cAMP-mediated activation of PKA. The inhibitory effect of TSP-1 on cAMP signaling could be reproduced with a peptide possessing a CD36 binding sequence of TSP-1, while the effects of TSP-1 were prevented by a CD36 blocking antibody. TSP-1 and the CD36 binding peptide induced phosphorylation of Src kinases, p38 and JNK. Moreover, inhibition of Src kinases blocked TSP-1-mediated regulation of cAMP concentrations and the phosphorylation of VASP, indicating that TSP-1 modulated the cAMP/PKA signaling events through a tyrosine kinase-dependent pathway downstream of CD36. These data reveal a new role for TSP-1 in promoting platelet aggregation through modulation of the cAMP-PKA signaling pathway.
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Books on the topic "Human platelet antigens"

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Macdougall, Iain C. Clinical aspects and overview of renal anaemia. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0123.

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Anaemia is an almost ubiquitous complication of chronic kidney disease, which has a number of implications for the patient. It is associated with adverse outcomes, an increased rate of red cell transfusions, poor quality of life, and reduced physical capacity. Severe anaemia also impacts on cardiac function, as well as on platelet function, the latter contributing to the bleeding diathesis of uraemia. Renal anaemia occurs mainly in the later stages of chronic kidney disease (stages 3B, 4, and 5), and up to 95% of patients on dialysis suffer from this condition. It is caused largely by inappropriately low erythropoietin levels, but other factors such as a shortened red cell survival also play a part. The anaemia is usually normochromic and normocytic, unless concomitant iron deficiency is present. The latter is also common in renal failure, partly due to low dietary iron intake and absorption, and partly due to increased iron losses. Prior to the 1990s, treatment options were limited, and many patients (particularly those on haemodialysis) required regular blood transfusions, resulting in iron overload and human leucocyte antigen sensitization. Correction of anaemia requires two main treatment strategies: increased stimulation of erythropoiesis, and maintenance of an adequate iron supply to the bone marrow. Ever since the introduction of recombinant human erythropoietin, it has been possible to boost erythropoietic activity, and both oral and intravenous iron products are available to provide supplemental iron. In dialysis patients, oral iron is usually poorly absorbed due to upregulation of hepcidin activity, and intravenous iron is often required. The physiological processes relevant to red cell production are described, as well as the prevalence, characteristics, pathogenesis, and physiological consequences of renal anaemia.
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Book chapters on the topic "Human platelet antigens"

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Bertrand, Gerald, and Fabiana Conti. "Genotyping of Human Platelet Antigens by BeadChip Microarray Technology." In Molecular Typing of Blood Cell Antigens, 149–65. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2690-9_13.

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Meyer, Stefan, Nadine Trost, Beat M. Frey, and Christoph Gassner. "Parallel Donor Genotyping for 46 Selected Blood Group and 4 Human Platelet Antigens Using High-Throughput MALDI-TOF Mass Spectrometry." In Molecular Typing of Blood Cell Antigens, 51–70. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2690-9_5.

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Bertrand, Gerald, and Cecile Kaplan-Gouet. "Human Platelet Antigen Genotyping and Diagnosis of Antiplatelet Alloimmunization." In BeadChip Molecular Immunohematology, 73–81. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-7512-6_6.

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McBride, Simon E. "Real-Time PCR Assays for High-Throughput Human Platelet Antigen Typing." In DNA and RNA Profiling in Human Blood, 39–49. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-553-4_4.

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Nauck, Markus S., Hedi Gierens, Matthias A. Nauck, Winfried März, and Heinrich Wieland. "Rapid, Homogeneous Genotyping of Human Platelet Antigen 1 by Fluorescence Resonance Energy Transfer and Probe Melting Curves." In Rapid Cycle Real-Time PCR, 273–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-59524-0_29.

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Avecilla, Scott T. "Human Platelet Antigens." In Transfusion Medicine and Hemostasis, 185–89. Elsevier, 2013. http://dx.doi.org/10.1016/b978-0-12-397164-7.00029-x.

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Kunicki, Thomas J., and Diane J. Nugent. "Human Platelet Antigens." In Blood Banking and Transfusion Medicine, 112–28. Elsevier, 2007. http://dx.doi.org/10.1016/b978-0-443-06981-9.50014-4.

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Avecilla, Scott T. "Human Platelet Antigens." In Transfusion Medicine and Hemostasis, 185–89. Elsevier, 2019. http://dx.doi.org/10.1016/b978-0-12-813726-0.00031-3.

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Beardsley, Diana S. "Identification of platelet membrane target antigens for human antibodies by immunoblotting." In Methods in Enzymology, 428–40. Elsevier, 1992. http://dx.doi.org/10.1016/0076-6879(92)15083-o.

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"roles of carrier proteins. The identification and usefulness of blood group antigens as markers will be described and possible explanations for their variation in expression will be discussed. Most red cell antigens have been investigated because they are clinically important [1]. The antibodies to some antigens have caused haemolytic disease of the newborn and/or transfusion reactions. Other antigens are involved in haemolytic anaemia and some are important in transplantation. Red cell antigens provided a tool for investigation of the red cell surface and for use as genetic, immunological and biochemical markers. More than 500 red cell antigens are serologically defined, about half of which have been officially recognised and have been numbered by the International Society of Blood Transfusion Working Party on Terminology for Red Cell Surface Antigens [2,3]. Antigens are divided into systems (antigens controlled by a locus or closely linked loci) and three holding files: collections (related antigens whose genetic relationship is unknown), antigens of high incidence or antigens of low incidence. THE MAIEA TECHNIQUE Sometimes if an antigen has a very high or a very low incidence it is hard to relate it to other antigens or to assign it to a system. Immunochemical studies and in the case of high incidence antigens, use of cells of rare phenotype can be informative and recently the MAIEA technique, monoclonal antibody specific immobilisation of erythrocyte antigens, has proved useful. MAIEA was an adaptation of a technique, MAIPA, frequently used for studying platelets. MAIEA can be used to assign red cells antigens, as recognised by human alloantisera, to particular components of the red cell membrane [4]. Location of antigens on specific red cell membrane components The Knops system consists of 4 high incidence antigens Kna, McCa, Sla and Yka with frequencies greater than 90% in populations tested. There is also a low incidence antigen Knb found in Whites [3]. The antibodies to these public antigens are difficult to identify serologically. The antigens show a wide variation of strength on different donor’s cells. There is a null phenotype, the Helgeson phenotype, which appears from serological tests to lack all 4 antigens [5]. Cells which lack one Knops antigen may have weakened expression of other Knops antigens. The mists about these serologically difficult antigens were cleared when Moulds et al [6] and Rao et al [7] independently showed that these antigens were carried on the CR1 (complement receptor 1, CD35) protein. The related antigen Csa was not located on CR1, so Csa and Csb were left in the Cost collection [3]." In Transfusion Immunology and Medicine, 188. CRC Press, 1995. http://dx.doi.org/10.1201/9781482273441-7.

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Conference papers on the topic "Human platelet antigens"

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Kieffer, N., M. Titeux, A. Henri, J. Breton-Gorius, and W. Vainchenker. "MEGAKARYOCYTIC ORIGIN OF PLATELET HLA CLASS I ANTIGEN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643546.

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The existence of HLA class I antigens on human platelets is well established. However, several authors have suggested that platelet HLA antigens are not integral membrane components but are acquired from soluble plasma sources and adsorbed to the platelet surface.In the present study, we used the monoclonal antibody W6/32, directed against a monomorphic epitope of the HLA class I antigen for the immunochemical characterization of platelet HLA. Immunoprecipitation experiments, performed after in vitro metabolic radiolabeling of human platelets revealed a band of molecular weight 44,000 identical to that precipitated from metabolic labeled U937 or HEL cells. When the same antibody was tested by indirected immunofluorescence in a double labeling technique on in vitro cultures of human megakaryocytes, performed in the absence of human serum in the culture medium, megakaryocytes identified by an anti-vWF MoAb revealed a membrane staining with W6/32 identical to that observed on other bone marrow cells, e.g. macrophages. Our results provide evidence that platelet HLA has a megaka-ryocytic origin and that residual biosynthesis of HLA antigen does still occur in circulating platelets. However, our results do not exclude the ability of human platelets to adsord circulating HLA class I antigen from plasma.
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Pereira, J., C. Cretney, and R. H. Aster. "VARIABLE EXPRESSION OF ALLOANTIGENS IN PLATELET COHORTS OF DIFFERENT MEAN DENSITY:AN EFFECT OF AGING IN VIVO." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644158.

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Platelets differ widely in size and density, but the relationship of this heterogeneity to platelet age and function is not established. Published evidence suggests that platelet alloantigens of the HLA and PlA systems may be acquired by or releasedfrom platelets in the circulation. We therefore studied expression of HLA, PlAl, and other markers in platelet cohorts of high density (HD) and low density (LD) separated on a linear, isoosmotic arabinogalactan gradient. HD and LD cohorts contained 11-14% of total platelets and did not differ significantly in mean cell volume. Alloantibodies reactive with antigens P1A1, Baka, and HLA-A2 were used to saturate alloantigen sites. Surface markers were quantified (Human Immunol. 15:251, 1986) with radiolabeled monoclonalprobes specific for HLA A, B, C antigens (W6/32), the Fc fragment of IgG (Hb-43) and the glycoprotein IIb/IIIa complex (AP-2).As shown in the Table, HD platelets carry significantly more PlAl (located on GPIIIa) and significantly less HLA than LD platelets. However, HD and LD cohorts express the same number of GPIIb/IIIa and Baka (located on GPIIb) molecules. These findings are consistent with preferential loss of HLA molecules from HD- platelets in the circulation or acquisition by LD platelets. The variable expression of P1A1 in HD and LD cohorts is apparently due to a conformational change in GPIIIa, rather than acquisition or loss of the GPIIIa molecule, because total GPIIb/IIIa was thesame in the two platelet populations. Whether antigen differences in HD and LD platelets are determined at the time of platelet production or result from aging of platelets in the circulation is under investigation.
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Wautier, J. L., Y. Gruel, B. Boizard, J. P. Caen, F. Daffos, and F. Forestier. "ANTENATAL DIAGNOSIS OF THROMBOPATHY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644271.

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We previously determined platelet antigens and glycoproteins in the human fetus after 19 weeks of intrauterine life (Blood 68, 488-92,1986). These results obtained in fetuses with normal platelets allowed us to do the first attempt of antenatal diagnosis in Glanzmann thrombasthenia. The fetal propositus was tested with monoclonal (AP2, AP3) or polyclonalantibodies (IgGL) directed against GPIIbllla or platelets antigen (PLA1, Leka). The foetus was found to be heterozygous for GT and similar results were foundafter his birth.Grey platelet syndrome is a rare congenital platelet defect caracterized by an alpha granule deficiency and is transmitted on the dominant feature. To be able to detect this abnormality before birth we have measured the platelet content of alpha granules.The amount of Beta thromboglobulin (gTG) at 18 weeks of intrauterine life was32±4.3 mg/109 platelets in normal platelets (adults 60 mg/10^ platelets). The foetus of the mother with grey platelet syndrome was sampled at 19 weeks when the mother was under platelet transfusion and the platelets were studied by electron microscopy and for their BTG content. The platelet morphologyshowed the presence of alpha granules and the $TG content was in the range of the control fetuses (42mg/109 platelets). The baby was born after artificial delivery under platelet transfusion. These results showed that the antenatal diagnosis of thrombopathies is feasible and can permit a therapy to avoid dramatic haemorrhage during pregnancy or delivery.
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Kawai, Y., R. R. Montgomery, K. Furihata, and T. J. Kunicki. "EXPRESSION OF PLATELET ALLOANTIGENS ON HUMAN ENDOTHELIAL CELLS AND HEL CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642813.

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Analogs of platelet membrane glycoproteins IIb and IIIa (GPIIb-IIIa) have been shown to be synthesized and expressed by human endothelial cells (HEC), a human erythroleukemia cell line (HEL) and various other cells. Previous studies from our laboratory demonstrated that the platelet alloantigen P1A1, is expressed on HEC GPIIIa. Other alloantigen systems, namely, Pen and Bak, are known to be localized on platelet GPIIIa and GPIIb, respectively. Utilizing additional antibodies from patients with PTP specific for Pena, Baka, and Bakb allo-antigens, and isoantibodies (iso-ab) from a patient with Glanzmann's Thrombasthenia (GT), we have studied cultured HEC and HEL cells for expression of epitopes recognized by these antibodies. HEC and HEL cells were meta-bolically labeled with 35S-methionine and lysed in 0.5% TX-100 in the presence of 5mM EDTA. Soluble antigens were immunoprecipitated with these antibodies coupled to Protein A-Sepharose and subjected to SDS-PAGE and fluorography. Anti-Pena and the GT iso-ab reacted with the GPIIb-IIIa complex from both HEC and HEL lysates, but anti-Baka and anti-Bakb failed to immunoprecipitate GPIIb-IIIa analogs from either HEC or HEL. In an immunoblot assay, the GT iso-ab bound to GPIIIa of both HEC and HEL. Anti-Pena failed to react with SDS-denatured proteins. HEL GPIIIa migrates slightly faster than HEC GPIIIa and slightly slower than platelet GPIIIa. These results indicate that the epitopes of platelet GPIIIa recognized by alloantibodies and isoantibodies are shared by GPIIIa analogs of HEC and HEL. GPIIb-associated alloantigens are not expressed by HEC and HEL GPIIb analogs, an observation that is consistent with the decreased structural homology between GPIIb analogs derived from different cell types.
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Kiefel, V., S. Santoso, and C. Mueller-Eckhardt. "ANALYSIS OF PLATELET REACTIVE ANTIBODIES USING MONOCLONAL ANTIBODIES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643929.

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The characterization of platelet reactive alloantibodies and autoantibodies is mandatory for the diagnosis of posttransfusion purpura, neonatal alloimmune thrombocytopenia, autoimmune thrombocytopenia and for the selection of platelet donors prior to platelet transfusions in immunized polytransfused patients. The platelet immunofluorescence test is suitable for the detection of platelet reactive antibodies. In many cases, however, mixtures containing different platelet reactive antibodies have to be dissected.In order to analyze these sera, we have developed a novel enzyme immunoassay based upon monoclonal antibody specific immobilization of platelet antigens (MAIPA). In brief, platelets are incubated simultaneously with the (human) serum to be investigated and a monoclonal (mouse) antibody directed against an epitope on the same platelet membrane glycoprotein (GP). Platelets are then washed and solubilized in TRIS buffered saline containing NP40. The lysed platelets are then pipetted into the wells of microtiter plates, coated with goat anti mouse IgG where mouse anti GP-complexes are immobilized. Human platelet reactive antibodies on the same GP are detected using enzyme labelled goat anti human IgG, IgM, or IgA, respectively. Using mab Gi5, mab FMC25, mab w6.32 directed against epitopes on the glycoprotein complex IIb/IIIa, glycoprotein Ib and HLA class I molecule, respectively, and a panel of typed platelet donors, even sera containing different platelet reactive antibodies are readily analyzed. Results of experiments with platelet specific alloantibodies (anti P1A1, anti P1A2 and anti Bak(a)), autoantibodies (against the GP Ilb/IIIa complex and GP Ib) and a drug dependent antibody show that this assay allows to discriminate all these different platelet reactive antibodies.
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Christie, D. J., S. S. Lennon, and L. L. Wischnack. "QUININE CAN INHIBIT OR ENHANCE PRODUCTION OF MURINE ANTI-HUMAN PLATELET ANTIBODIES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644577.

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Quinine (Qn) can provoke potent antibodies capable of destroying platelets and inducing life-threatening immunologic thrombocytopenia (DITP). A question critical to understanding the mechanism of DITP is why do platelets from all normal individuals express Qn-induced antigens while only relatively few individuals make the destructive drug-dependent antibodies? This problem was investigated in a murine animal model. BALB/c mice (6-12wk) were injected intraperitoneally, every other week, with saline or lOOOpg of Qn (this dose of drug gave serum levels comparable to human therapeutic serum levels). Two wk after the second injection, mice were immunized with a single dose of 108 human platelets and either 0 or 1000μg of Qn. One wk later, mouse serum was screened in the presence and absence of drug for anti-platelet activity by a complement-dependent 51Cr release assay. Results are shown in the table and represent data from at least 2 groups of five mice each.Antibody titers were more than 10-fold lower in mice receiving 1000 |lg Qn than in mice injected with platelets alone. In contrast, mice repeatedly immunized (3-6 injections) with platelets and low doses of Qn (20μg) developed enhanced antibody activity (drug-dependent and nondrug-dependent) that consistently titered two-to four-fold higher than mice injected with platelets alone. Results were confirmed by an enzyme-linked immunosorbent assay which showed that the murine antibodies were IgG. These findings demonstrate that by varying the dose, Qn can either inhibit or enhance production of anti-human platelet antibodies in mice. This suggests the possibility that most individuals fail to respond to Qn because therapeutic doses of the drug inhibit antibody formation; yet in individuals capable of responding, even low doses of Qn (as found in tonic water) can enhance production of antibodies that provoke DITP.
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Pidard, D., A. Fischer, C. Bouillot, F. Ledeist, and A. T. Nurden. "INHERITED DEFICIENCIESCAN AFFECT SEPARATELY THE PLATELET MEMBRANE GLYCOPROTEIN Ilb-IIIa COMPLEX AND THE LEUKOCYTE LFA-1, Mac-1 and pl50,95 COMPLEXES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643704.

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The human platelet membrane glycoprotein (GP) IIb-IIIa complex and a family of functional leukocyte cell membrane antigens, LFA-1 (L), Mac-1 (M) andpl50,95 (X), possess knownstructural analogies. Similaritiesinclude a heterodimeric structure with a high mol. wt. αsubunit (Mr∽ 145-180 kDa) , associated nonconvalently with a lower mol. wt.β-subunit (Mr ∽ 90-95 kDa),anda partial amino acid sequence hommology between GP lib and αL or CKM. Furthermore, GP lib, α L and αM were reported to be co-expressed in murine cells transfected with a 20 kilobase human DNA fragment.To address the question of a possible genomic linkage between these related glycoproteins of different cells, we have examined patients with either ‘LFA-1 immunodeficiency disease’ or with Glanzmann's thrombasthenia (GT). S.Bo. and P.Ce. are children affected by recurrent bacterial infections since birth. Cytofluorimetric analysis using monoclonal antibodies (MAbs) for the αL, αM,αX and β subunits demonstrated that the surface expression of LFA-1, Mac-1 and pl50,95 intheir leukocytes was ≤1% of the normal values. Platelets from both patients aggregated normally and readily bound the MAbs AP-2 (anti-GP IIb-IIIa) or Tab (anti-GP IIb). Crossed immunoelectrophoresis confirmed the presenceof GP IIb-IIIa complexes, whileSDS-polyacrylamide gel electrophoresis showed a normal migration of GP IIb and GP IIIa. Patients C. Bl. and M.Ca.are typical of the type I subgroupofGT. Their platelets are unable toaggregate and contain < 1% of the normal platelet content of GP liband GP Ilia.Cytofluoro-graphy showed a normal expression of LFA-1, Mac-1 and 150,95 on the surface of lymphocytes, polymorphonuclear cells and/or monocytes of both patients. Our data thus show that despite sequence homologies and a potential genomic linkage, the cellular expression of the platelet GP IIb-IIIa complex and of the LFA-1 related leukocyte antigens may be dissociated in genetic disorders where anabnormal glycoprotein distribution may be restricted to one type of cell.
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Cramer, Elisabeth M., F. John, William Vainchenker, and Janine Breton-Gorius. "PRODUCTION AND LOCALISATION OF ALPHA-GRANULE PROTEINS IN MATURING MEGAKARYOCYTES: AN OVERVIEW ON ULTRA-STRUCTURAL ASPECTS OF MEGAKARYOCYTE MATURATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642952.

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In order to study the production of α- granule proteins in maturing megakaryocytes, we used immunocytochemical techniques performed on cultured and enriched bone marrow megakaryocytes. Cultures were prepared from bone marrow CFU-MK with the methylcellulose and plasma clot techniques. Preparation of bone marrow megakaryocytes was carried out from human or pig rib marrow separated on percoll gradient and counterflow centrifugation. Megakaryocyte preparations were 90$ pure and represented 85$ of those in the whole marrow. Activation was prevented with prostacyclin and prefixation with low concentration glutaraldehyde. A panel of monoclonal and polyclonal antibodies, against different platelet membrane glycoproteins and against cytoplasmic antigens (such as von Willebrand Factor (vWF), fibrinogen (Fg) and thrombospondin (TSP)) was used and observed by immunofluorescence or by immunogold in electron microscopy.The first megakaryocytic precursors, promegakaryoblasts (PMKB) identifiable by these antibodies were found at day 5 of culture. They had the size of lymphocytes, were labelled for GP lib, Ilia, and Ilb-IIIa complex but not for GPIb which appeared later. Platelet peroxidase was also present, otherwise these cells were devoid of α- granules and only a few of them exhibited a diffuse pattern for vWF immunolabelling. One day later membrane GPIb and diffuse cytoplasmic labelling for vWF were detected in the majority of PMKB. At day 9 of culture, this pattern of labelling for vWF became more intense and granular. The same pattern was observed for TSP and platelet factor 4. Immunoelectron microscopy showed that in immature megakaryocytes isolated from human bone marrow, labelling for vWF and TSP was observed in vesicles located in the Golgi region; in addition numerous small granules less than 0.1pm in diameter, round or elongated in shape, were labelled for these antigens. In mature human megakaryocytes, the labelling for these cytoplasmic antigens was restricted to the platelet α- granules in a distribution pattern similar to that of platelet α- granules. However, the labelling for Fg was consistently less intense in the granules of immature and mature megakaryocytes than in platelets.Because in platelets α- granule immunolabelling for vWF is associated with tubular structures which are specially prominent in porcine species, we studied vWF and tubular structures in pig megakaryocytes. Standard and immunoelectron microscopy revealed the simultaneous appearance of both in the small vesicles located in the Golgi area in the small immature α- granules and later in the mature α- granules. In mature megakaryocytes, labelling for vWF was intense and restricted to the α- granules. It was distributed eccentrically as in porcine blood platelets. Gold particles were often eccentrically located at one pole of the α- granule either labelling only its periphery or outlining one side of an elongated granule. Standard electron microscopy showed that tubular structures were very numerous in the mature α-granules, regularly spaced, arranged in parallel and usually located at one side of the granule. On the other hand platelets from pigs with homozygous von Willebrand disease were found to be completely devoid of both tubular structures and immunolabelling for vWF suggesting that the tubules represent the vWF itself.In acute megakaryoblastic leukemia, several phenotypes of PMKB were found in different patients, which corresponded to the stages of maturation of cultured megakaryocytes from CFU-MK.In conclusion, immunolabelling methods combined with megakaryocyte enrichment techniques are useful tools to study the origin of megakaryocyte (and platelet) granular proteins.
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Toti, F., A. Stierlé, M. L. Wiesel, A. Schwartz, J. M. Freyssinet, and J. P. Cazenave. "PRODUCTION OF ANTIBODIES TO HUMAN VON WILLEBRAND FACTOR IN LAYING HENS. ISOLATION OF IMMUNOGLOBULINS AND APPLICATIONS TO THE DETECTION OF MOLECULAR DEFECTS OF VON WILLEBRAND FACTOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644084.

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Von Willebrand disease (vWD) is an inherited disorder of primary hemostasis caused by deficiency or structural abnormalities of von Willebrand factor (vWF). VWF circulates in plasma and is also present in platelets. Plasma vWF, the carrier protein for factor VIII, is a large multimeric glycoprotein composed of identical subunits linked by disulfide bridges. Plasma and platelet vWF display distinct multimeric electrophoretic patterns. The different vWD subtypes can be classified either by the determination of vWFantigen (vWFíAg) and/or by multimer distribution. Antibodies to human vWF were raised in laying hens by intramuscular injections of purified human vWF. Immunoglobulins were isolated from egg yolks by selective polyethylene glycol and ammonium sulfate precipitations. These antibodies appeared to be monospecific, as they did not react with the plasma proteins of a patient with severe vWD. The pullets received weekly 50 μg vWF for 4 weeks and then had monthly injections. The antibodies occurred as early as the third injection, the yield being 300 to 500 mg of immunoglobulin per week (6-7 eggs). The titre could be constant over periods greater than 1 year. These immunoglobulins to vWF were tested in vWFíAg electroimmunoassays and for the multimer analysis of plasma and platelet vWF by electrophoresis and immunoblotting techniques. In no case could a difference be detected between assays performed with rabbit monospecific antiserum or with yolk immunoglobulins to human vWF. Ten to 12 multimers could be revealed for normal plasma vWF and up to 12 to 14 bands for normal platelet vWF (1.7% agarose). In the case of vWD, the electrophoresis patterns were identical with both antibodies. Thus, antibodies to vWF raised in laying hens are a suitable tool to detect and to characterize vWD. Although they do not interact with protein A, yolk antibodies are certainly advantageous to produce, as they do not contain IgM or IgA. Immunoglobulin fractions can contain up to 10 % of specific antibodies. Since they are available in larger quantities and are easy to isolate, larger homogeneous batches of antibodies can be obtained. This method may easily be applied to develop antibodies to a variety of antigens.
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Kieffer, N., L. Edelman, P. Edelman, C. Legrand, J. Breton-Gori us, and W. Vainchenker. "A MONOCLONAL ANTIBODY AGAINST AN ERYTHROID ONTOGENIC ANTIGEN IDENTIFIES GP IV ON HUMAN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643532.

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A murine monoclonal antibody (FA6-152), obtained by immunizing mice with fetal human erythrocytes agglutinated fetal but not adult erythrocytes and bound to both adultand fetal monocytes, platelets andreticulocytes. The antibody did not react with lymphocytes or granulocytes (P. Edelman et al., Blood, 1986, 67, 56). Fluorescent labeling of marrow cells and of in vitro BFU-E, CFU-GM and CFU-MK derivedcolonies revealed that the antigen defined by FA6 was absent from the granulocytic precursors and was detected on the megakaryo-cytic lineage at a later stage of differentiation than major platelet membraneglycoprotein markers. In contrast,the antigen appeared as a very early marker of erythroid differentiation.In the present report, we performed immunoprecipitation experiments on surface labeled platelets toidentify the platelet FA6 antigen.A band of apparent Mr - 85,000 wasimmunoprecipitated from iodinated platelets. This band was also revealed after periodate/Na[3H]BH4 orneuraminidase galactose oxidase/Na[3H]BH4 surface labeling of the platelets, providing evidence that the FA6 antigen corresponds to platelet GP IV. Preliminary studies revealed that FA6-IgG inhibited platelet aggregation induced by low doses of thrombin without affecting the platelet release reaction. Our results therefore suggest that GP IV, which isa multi-lineage hematopoietic differentiation marker, could play a role in cell-cell or cell-substrateinteractions common to different hematopoietic cell types.
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