Genetic variations of <i><scp>CD</scp>36</i> and low platelet <scp>CD</scp>36 expression – a risk factor for lipemic plasma donation in Taiwanese apheresis donors

Lo, Su Shun; Lin, Kuan-Hsiao; Hsieh, Hwei Ho; Lin, Dong-Tasmn; Hu, Chung-Yi

doi:10.1111/vox.12356

Cited by 9 publications

(12 citation statements)

References 27 publications

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“…24 The mutation of six nucleotide deletions (1254 1 6_1254 1 11delTATTTG) seems to be a rare mutation among the Taiwanese population (allele frequency 5 0.00078). 21 Lo and colleagues have also reported one Taiwanese individual who had low CD36 expression on platelets. This individual was heterozygous, carrying both wild-type and mutant alleles.…”

Section: Discussionmentioning

confidence: 97%

“…19,20 More recently, Lo and coworkers reported that 0.6% of Taiwanese fail to express CD36 on both platelets and monocytes (Type I CD36 deficient; CD36null). 21 It is known that…”

Section: Discussionmentioning

confidence: 99%

“…In Taiwan, recent studies have demonstrated that the HPA incompatibility between fetus and mother leading to the production of maternal anti‐HPA alloantibodies is mostly in the HPA‐3, HPA‐5, and HPA‐15 systems . More recently, Lo and coworkers reported that 0.6% of Taiwanese fail to express CD36 on both platelets and monocytes (Type I CD36 deficient; CD36 null ) . It is known that CD36 null mothers can produce anti‐CD36 isoantibodies during pregnancy, leading to the destruction of fetal platelets, known as FNAIT syndrome …”

Section: Discussionmentioning

confidence: 99%

“…The total absence of CD36 expression on monocytes as well as platelets in this mother could be attributed to heterozygous deletions: 332_333del CA and 1254 + 6_1254 + 11delTATTTG in Exon 5 and Intron 13, respectively. The dinucleotide deletion 329‐330delAC represents the most frequent mutation found in Taiwanese and Chinese populations leading to frameshift at Position 110 . The mutation of six nucleotide deletions (1254 + 6_1254 + 11delTATTTG) seems to be a rare mutation among the Taiwanese population (allele frequency = 0.00078) .…”

Section: Discussionmentioning

confidence: 99%

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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: Discussionmentioning

confidence: 97%

“…19,20 More recently, Lo and coworkers reported that 0.6% of Taiwanese fail to express CD36 on both platelets and monocytes (Type I CD36 deficient; CD36null). 21 It is known that…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

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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“…The most frequent mutations are c.975T>G in African, c.268C>T and c.329_330del in Japanese, and c.329_330del and c.1228_1239del in Chinese populations. In a study by Lo et al, 19 the population in three classes of CD36 expression was classified—CD36 WT , CD36 low , and CD36 null , depending on their level of expression—and they tried to make a correlation with CD36 genetic variations: for two of four patients with Type I CD36 deficiencies (CD36 null ) they observed only one mutated allele, whereas the two other cases were, as commonly described, homozygous or compound heterozygous. Similarly, in our experience, we sequenced DNA for eight patients with Type I CD36 deficiency (including four SCD patients), and we observed for five of them only one heterozygous mutation (data not shown), the second event being still unknown and under investigation.…”

Section: Discussionmentioning

confidence: 99%

New molecular basis associated with CD36‐negative phenotype in the sub‐Saharan African population

et al. 2020

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Background: CD36 glycoprotein is expressed by various cell types, including platelets (PLTs), monocytes, and erythroid precursors, and is also the receptor for several ligands. However, absence of CD36 expression seems asymptomatic and is poorly described in Caucasians. In contrast, the frequency reaches 7% and 11% in African Caribbean and Asian persons, respectively. Lack of CD36 expression exposes to the risk of immunization in case of pregnancy or PLT transfusion. Two types of deficiency have been described: in Type I, PLTs and monocytes lack CD36 expression and the subjects are homozygous or compound heterozygous for CD36 mutations, whereas in Type II, only PLTs (Type IIa), and rarely also erythroid cells (Type IIb), are affected. Molecular events leading to Type II deficiency are poorly understood. Case Report: An African girl, diagnosed with homozygous sickle cell disease and regularly transfused, was assessed for PLT CD36 expression by immunofluorescence microscopy. The deficiency was then confirmed by monoclonal antibody immobilization of PLT antigen (MAIPA) assay, and the subtype was

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Thromboelastography characterized CD36 null subjects as slow clot formation and indicative of hypocoagulability

Lee

Lin²,

et al. 2019

Thrombosis Research

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Genetic variations of CD36 and low platelet CD36 expression – a risk factor for lipemic plasma donation in Taiwanese apheresis donors

Abstract: Through this study, we established a donor registry to supply CD36-negative platelets for patients in need.

Cited by 9 publications

References 27 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

New molecular basis associated with CD36‐negative phenotype in the sub‐Saharan African population

Thromboelastography characterized CD36 null subjects as slow clot formation and indicative of hypocoagulability

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