Improvement of Anti-CD36 Antibody Detection via Monoclonal Antibody Immobilization of Platelet Antigens Assay by Using Selected Monoclonal Antibodies

Xu, Xiuzhang; Chen, Dawei; Ye, Xin; Xia, Wenjie; Shao, Yuan; Deng, Jing; Chen, Yangkai; Ding, Haoqiang; Liu, Jing; Xu, Yaori; Fu, Yongshui

doi:10.3343/alm.2023.43.1.86

Cited by 3 publications

(1 citation statement)

References 25 publications

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“…CD36 deficiency is divided into two groups: type I deficiency, which is characterized by lack of CD36 expression on platelets and all other cells [6, 7] and type II, in which CD36 expression is lacking from platelets only [8, 9]. CD36 deficiency type I, while rare in Europeans, occurs with a prevalence of approximately 3% in Africans [10], 0.5%–1% among the Japanese [11, 12] and 0.5% in China [13], as recently summarized by Xu et al [14]. Type I deficiency is of clinical significance since it can be considered a null phenotype associated with the development of antibodies against CD36.…”

Section: Introductionmentioning

confidence: 99%

Evidence that CD36 is expressed on red blood cells and constitutes a novel blood group system of clinical importance

Alattar,

Storry,

Olsson

2024

Vox Sanguinis

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Background and ObjectivesPolymorphic molecules expressed on the surface of certain blood cells are traditionally categorized as blood groups and human platelet or neutrophil antigens. CD36 is widely considered a platelet antigen (Naka) and anti‐CD36 can cause foetal/neonatal alloimmune thrombocytopenia (FNAIT) in CD36‐negative pregnant women. CD36 is used as a marker of differentiation in early erythroid culture. During the experimental culture of CD34+ cells from random blood donors, we observed that one individual lacked CD36. We sought to investigate this observation further and determine if CD36 fulfils the International Society of Blood Transfusion criteria for becoming a blood group.Materials and MethodsSurface markers were monitored by flow cytometry on developing cells during the erythroid culture of CD34+ cells. Genetic and flow cytometric analyses on peripheral blood cells were performed. Proteomic datasets were analysed, and clinical case reports involving anti‐CD36 and foetal anaemia were scrutinized.ResultsSequencing of CD36‐cDNA identified homozygosity for c.1133G>T/p.Gly378Val in the CD36‐negative donor. The minor allele frequency of rs146027667:T is 0.1% globally and results in abolished CD36 expression. CD36 has been considered absent from mature red blood cells (RBCs); however, we detected CD36 expression on RBCs and reticulocytes from 20 blood donors. By mining reticulocyte and RBC datasets, we found evidence for CD36‐derived peptides enriched in the membrane fractions. Finally, our literature review revealed severe cases of foetal anaemia attributed to anti‐CD36.ConclusionsBased on these findings, we conclude that CD36 fulfils the criteria for becoming a new blood group system and that anti‐CD36 is implicated not only in FNAIT but also foetal anaemia.

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Section: Introductionmentioning

confidence: 99%

Evidence that CD36 is expressed on red blood cells and constitutes a novel blood group system of clinical importance

Alattar,

Storry,

Olsson

2024

Vox Sanguinis

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Haplotypes analysis reveals the genetic basis of type I CD36 deficiency

Xia,

Chen,

et al. 2024

Sci Rep

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CD36, also known as glycoprotein IV, is classified into two distinct subgroups based on the presence or absence of its expression on monocytes. The CD36 gene spans approximately 50,000 base pairs. Historically, research has focused on identifying CD36 mutations through Sanger sequencing and next-generation sequencing (NGS), with limited exploration of haplotypes. In this study, we collected blood samples from donors with type I and type II CD36 deficiencies as well as from healthy controls, and employed single-molecule long-read sequencing (also known as Third-Generation Sequencing) of genomic DNA to analyze the genetic basis of CD36. The study identified 180 genetic variants, 12 of which were found to alter the amino acid sequence. Notably, four of these mutations (c.220 C > T; c.329_330delAC; c.430-1 G > C; c.1006 + 2 T > G) are premature termination mutations that lead to protein truncation. Using Fisher’s exact test, we statistically analyzed a specific haplotype, c.-132A > C and c.329_330delAC, along with their clinical phenotypes, revealing a strong association between these variants in the 5’ block and type I CD36 deficiency. We analyzed the CD36 gene sequences in platelet donors and patients with PTR (platelet transfusion refractoriness) and FNAIT (fetal and neonatal alloimmune thrombocytopenia), conducting a detailed haplotype analysis associated with type I CD36 deficiency and FNAIT. Supplementary Information The online version contains supplementary material available at 10.1038/s41598-024-74917-0.

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Update on transfusion-related acute lung injury: an overview of its pathogenesis and management

Lian

2023

Front. Immunol.

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Transfusion-related acute lung injury (TRALI) is a severe adverse event and a leading cause of transfusion-associated death. Its poor associated prognosis is due, in large part, to the current dearth of effective therapeutic strategies. Hence, an urgent need exists for effective management strategies for the prevention and treatment of associated lung edema. Recently, various preclinical and clinical studies have advanced the current knowledge regarding TRALI pathogenesis. In fact, the application of this knowledge to patient management has successfully decreased TRALI-associated morbidity. This article reviews the most relevant data and recent progress related to TRALI pathogenesis. Based on the existing two-hit theory, a novel three-step pathogenesis model composed of a priming step, pulmonary reaction, and effector phase is postulated to explain the process of TRALI. TRALI pathogenesis stage-specific management strategies based on clinical studies and preclinical models are summarized with an explication of their models of prevention and experimental drugs. The primary aim of this review is to provide useful insights regarding the underlying pathogenesis of TRALI to inform the development of preventive or therapeutic alternatives.

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Improvement of Anti-CD36 Antibody Detection via Monoclonal Antibody Immobilization of Platelet Antigens Assay by Using Selected Monoclonal Antibodies

Cited by 3 publications

References 25 publications

Evidence that CD36 is expressed on red blood cells and constitutes a novel blood group system of clinical importance

Evidence that CD36 is expressed on red blood cells and constitutes a novel blood group system of clinical importance

Haplotypes analysis reveals the genetic basis of type I CD36 deficiency

Update on transfusion-related acute lung injury: an overview of its pathogenesis and management

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