Quantitation of CD36 (platelet glycoprotein IV) expression on platelets and monocytes by flow cytometry: Application to the study of <i>Plasmodium falciparum</i> malaria

Cserti‐Gazdewich, Christine; Dzik, Walter H.; Dorn, Michelle E.; Quagliaroli, Robert O.; Xu, Songyi; Ssewanyana, Isaac; Nayyar, Rakesh; Preffer, Frederic I.

doi:10.1002/cyto.b.20443

Cited by 17 publications

(13 citation statements)

References 59 publications

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“…18 Briefly, 200 mL ethylene diamine tetra acetic acid (EDTA)-anticoagulated blood was incubated at room temperature for 30 minutes with 4 mL fluorescence-labeled monoclonal antibodies (Biolegend): allophycocyanin-conjugated anti-human CD36 (clone 5-271), fluorescein isothiocyanate (FITC)-labeled anti-human CD61 (clone VI-PL2), and phycoerythrin-conjugated antihuman CD14 (clone HCD14). After the addition of lysis solution (BD Biosciences), labeled cells were washed with 2 mL 10 mM EDTA/phosphate-buffered saline (PBS) and then fixed with 500 mL 1% paraformaldehyde in PBS/EDTA buffer.…”

Section: Genotyping Of Hpasmentioning

confidence: 99%

Fetal/neonatal alloimmune thrombocytopenia due to anti‐CD36 antibodies: antibody evaluations by CD36‐transfected cell lines

Lin

Lee

et al. 2017

Transfusion

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BACKGROUND: Isoantibodies against CD36 (platelet glycoprotein 4), developed in Type I CD36-deficient mothers are frequently reported as the cause of fetal/ neonatal alloimmune thrombocytopenia in the Asian population. Therefore, further detailed characterization of anti-CD36-mediated fetal/neonatal alloimmune thrombocytopenia is warranted. Here, we report the characterization of a patient with fetal/neonatal alloimmune thrombocytopenia in a Taiwanese family caused by anti-CD36 isoantibodies using a novel antigen-capture method. STUDY DESIGN AND METHODS:Platelets and monocytes were analyzed for CD36 expression by flow cytometry. Sequencing analysis of the CD36 gene was performed to identify the mutation underlying the CD36 deficiency. Stable transfected human embryonic kidney HEK293 cells expressing recombinant CD36 were established. These cells were used for the characterization of anti-CD36 isoantibodies by flow cytometry, immunoprecipitation, and antigen-capture assay. RESULTS:Flow cytometry analysis revealed a total absence of CD36 on both platelets and monocytes of the mother (Type I CD36-deficient) caused by heterozygous deletions of the CD36 gene (332_333delCA and c.1254 1 6_1254 1 11delTATTTG). Analysis of maternal serum with CD36-transfected HEK293 cells by flow cytometry, immunoprecipitation, and antigen-capture assay demonstrated the presence of anti-CD36 isoantibodies in maternal serum. Interestingly, this antibody could not be detected by the monoclonal antibody immobilization of platelet antigens assay when anti-CD36 monoclonal antibody (clone FA6-152) was used as the capture antibody.CONCLUSION: This case reemphasizes the role of anti-CD36 isoantibodies on the pathomechanism of fetal/ neonatal alloimmune thrombocytopenia. The fact that the monoclonal antibody immobilization of platelet antigens assay does not seem to be reliable for the identification of all anti-CD36 antibodies indicates that screening of anti-CD36 isoantibodies by a monoclonal antibody-independent method, as presented here, should be considered. Fetal/neonatal alloimmune thrombocytopenia (FNAIT), which occurs in from 1 of 800 to 1 of 1000 live births, is the most common cause of severe thrombocytopenia and intracranial hemorrhage in the fetus and in term newborns.1,2 FNAIT is caused by maternal antibodies, which recognize paternalderived alloantigens on fetal platelets, leading to platelet destruction. In Caucasians, more than 75% of FNAIT cases are induced by alloantibodies against human platelet antigen-1a (HPA-1a), 3,4 whereas the most common antibodies causing FNAIT in Japanese are anti-HPA-4b alloantibodies. The clinical importance of anti-CD36 isoantibodies in the development of FNAIT has been reported in different populations.9-13 Currently, the antigen-capture assay represents the gold standard for detecting platelet antibodies. 14 With this assay, platelet antigens captured by mouse monoclonal antibody are used as the target for platelet antibodies. Unfortunately, this approach does not seem to be reliable for the identi...

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Section: Genotyping Of Hpasmentioning

confidence: 99%

Fetal/neonatal alloimmune thrombocytopenia due to anti‐CD36 antibodies: antibody evaluations by CD36‐transfected cell lines

Lin

Lee

et al. 2017

Transfusion

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“…Specimens were run on a 3-laser FACSCanto (BD Biosciences, San Jose, CA) running DiVa 6.1.1 software; instrument calibration was performed and tested weekly as previously detailed (41). Whole bone marrow and hip marrow samples collected in EDTA anticoagulant were washed three times in phosphate-buffered saline (PBS) and resuspended with 1% bovine serum albumin in PBS.…”

Section: Flow Cytometrymentioning

confidence: 99%

Multiparameter immunophenotyping by flow cytometry in multiple myeloma: The diagnostic utility of defining ranges of normal antigenic expression in comparison to histology

Cannizzo

Bellio

Sohani

et al. 2010

Cytometry Part B Clinical

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Background: Numerous studies have reported on the immunophenotype of plasma cells (PCs) in monoclonal gammopathy of undetermined significance (MGUS) and in plasma cell myeloma (PCM), but very few have examined the immunophenotype of normal PCs. In this study, an objective definition of normal range of expression for each antigen was found on normal control PCs. Using these new ranges of normal expression (new method) is different from using a static 20% of PCs cut-off for all antigens as described in the literature (traditional method). These newly calculated normal ranges for each antigen were applied to our data, and compared to histologic and immunohistochemical findings.Methods: Bone marrow samples from 46 patients with PC neoplasms and 15 normal controls were studied. A minimum of 100 PC were analyzed for each patient and control sample. An 8-color staining method was applied to study the immunophenotype of PCs, using a BD FACSCanto II.Results: By the new ranges of normality calculated in this study it was determined that different antigens have different level of expression on polyclonal PCs. CD19 correlated with histology by both the traditional and new methods, but had superior correlation by the new method.Conclusions: This report is the first 8-color immunophenotypic study of PCM in which a ''range of normal expression'' for each antigen is defined. This is a critical step to help distinguish between a normal and neoplastic PC immunophenotype and discern which antigens are of diagnostic importance. V C 2010

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“…Within circulating blood, platelet CD36 may be especially relevant. Although CD36 expression per platelet is about one‐half that found per monocyte, platelets so out‐number monocytes that the largest biomass of CD36 in circulating blood is found on platelets [83].…”

Section: Section 3: Platelet Glycoprotein IV (Cd36) and Plasmodium Famentioning

confidence: 99%

Plasmodium falciparummalaria and the immunogenetics of ABO, HLA, and CD36 (platelet glycoprotein IV)

2010

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Plasmodium falciparum malaria has long been a killer of the young, and has selected for polymorphisms affecting not only erythrocytes, but the immunogenetics of three histocompatibility systems: ABO, human leukocyte antigen (HLA), and CD36. The ABO system is important because the original allele, encoding glycosylation with the A sugar, acts as an adhesion ligand with infected red blood cells (iRBC), thereby promoting vasoocclusion. The prevalence of blood group O, which reduces this cytoadhesion, has increased in endemic areas. Other adaptations which could mitigate A-mediated rosetting include weaker A expression and increased soluble A secretion. The role of the HLA system in malaria has been harder to verify. Although HLA-B53 and DRB1*04 may be associated with clinical outcome, HLA studies are challenged by numerous comparisons in this most polymorphic of systems, and confounded by increasingly heterogeneous populations. Certain HLA markers may also reflect linkage artefact with other malaria-relevant polymorphisms. HLA may be less important because the parasite predominantly invades a compartment which does not express HLA. Adhesion of iRBCs is also mediated by CD36, expressed on platelets, monocytes, and microvascular endothelium. CD36 on monocytes is involved in clearing iRBC, while CD36 on platelets and the endothelium may play a role in tissue sequestration. The genetics of CD36 expression are complex, and recent research is fraught with inconsistent results. The solution may lie in examining genotype-phenotype correlations, zygosity effects on differential tissue expression, or other mechanisms altering CD36 tissue expression. Carefully designed prospective studies should bridge the gap between in-vitro observations and clinical outcomes.

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Quantitation of CD36 (platelet glycoprotein IV) expression on platelets and monocytes by flow cytometry: Application to the study of Plasmodium falciparum malaria

Cited by 17 publications

References 59 publications

Fetal/neonatal alloimmune thrombocytopenia due to anti‐CD36 antibodies: antibody evaluations by CD36‐transfected cell lines

Fetal/neonatal alloimmune thrombocytopenia due to anti‐CD36 antibodies: antibody evaluations by CD36‐transfected cell lines

Multiparameter immunophenotyping by flow cytometry in multiple myeloma: The diagnostic utility of defining ranges of normal antigenic expression in comparison to histology

Plasmodium falciparummalaria and the immunogenetics of ABO, HLA, and CD36 (platelet glycoprotein IV)

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