Frequency of human platelet antigens among blood donors in northeastern Thailand

Urwijitaroon, Yupa; Barusrux, Sahapat; Romphruk, Amornrat; Puapairoj, Chintana

doi:10.1046/j.1537-2995.1995.351096026370.x

Cited by 23 publications

(16 citation statements)

References 14 publications

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“…As a matter of fact, Brazilian Caucasians and those of African descent were clustered together, but not with the Amazonas blood donors. Furthermore, it has been observed that native Brazilian populations do not present the HPA‐1 b allele (Covas et al , ; Castro et al , ; Chiba et al , ), which is markedly similar to what has been described in Asian populations (Santoso et al , ; Kim et al , ; Urwijitaroon et al , ).…”

Section: Discussionsupporting

confidence: 65%

The human platelet alloantigen profile in blood donors from Amazonas, Brazil

Portela

Schriefer

Albuquerque

et al. 2016

Transfusion Medicine

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Section: Discussionsupporting

confidence: 65%

The human platelet alloantigen profile in blood donors from Amazonas, Brazil

Portela

Schriefer

Albuquerque

et al. 2016

Transfusion Medicine

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“…CD36 -mice have normal tail vein bleeding times and over many years of observation do not exhibit a bleeding diathesis. Human platelet CD36 deficiency (known as the Nak a-phenotype) is common in Asian and African populations (24)(25)(26)(27), and similar to the situation in mice, is not associated with an obvious bleeding diathesis. Recently our group, in collaboration with Podrez, Hazen, and Byzova, showed that atherogenic oxLDL binds and activates platelets in a CD36-dependent manner (28).…”

Section: Introductionmentioning

confidence: 99%

Platelet CD36 mediates interactions with endothelial cell–derived microparticles and contributes to thrombosis in mice

Li²,

et al. 2008

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CD36 is a scavenger receptor that binds multiple ligands, including phosphatidyl serine (PS). Although CD36 -mice do not have a bleeding diathesis, we show here that they do have significantly prolonged thrombotic occlusion times in response to FeCl 3 -induced vascular injury. Because cell-derived microparticles (MPs) are generated in response to vascular injury and circulate in patients with prothrombotic diseases, we hypothesized that PS exposed on their surfaces could be an endogenous CD36 ligand that transmits an activating signal to platelets. We found that MPs prepared from human ECs, monocytes, or platelets or isolated from blood of normal subjects bound to platelets. Binding was not observed with platelets from CD36 -donors and was inhibited by an anti-CD36 antibody or by blockade of exposed PS by annexin V or anti-PS IgM. Preincubation of platelets with MPs led to CD36-dependent augmentation of platelet activation in response to low doses of ADP, as assessed by measuring α 2b β 3 activation, P-selectin expression, and aggregation. Immunofluorescence confocal microscopy of murine carotid thrombi from CD36 -mice showed a significant decrement in endothelial antigen accumulation, which suggests that CD36 plays a role in MP recruitment into thrombi. These results provide what we believe to be a novel role for CD36 in thrombosis.

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“…CD36 deficiency (or Nak a -negative blood group) has been reported in Japanese (9), Thais (10) and African-Americans (11). The prevalence of CD36 deficiency in East Asian and African populations raises the possibility that the responsible variants have been selected for by malaria.…”

Section: Introductionmentioning

confidence: 99%

Positive selection of a CD36 nonsense variant in sub-Saharan Africa, but no association with severe malaria phenotypes

Fry

Ghansa

Small

et al. 2009

Human Molecular Genetics

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The prevalence of CD36 deficiency in East Asian and African populations suggests that the causal variants are under selection by severe malaria. Previous analysis of data from the International HapMap Project indicated that a CD36 haplotype bearing a nonsense mutation (T1264G; rs3211938) had undergone recent positive selection in the Yoruba of Nigeria. To investigate the global distribution of this putative selection event, we genotyped T1264G in 3420 individuals from 66 populations. We confirmed the high frequency of 1264G in the Yoruba (26%). However, the 1264G allele is less common in other African populations and absent from all non-African populations without recent African admixture. Using long-range linkage disequilibrium, we studied two West African groups in depth. Evidence for recent positive selection at the locus was demonstrable in the Yoruba, although not in Gambians. We screened 70 variants from across CD36 for an association with severe malaria phenotypes, employing a case–control study of 1350 subjects and a family study of 1288 parent–offspring trios. No marker was significantly associated with severe malaria. We focused on T1264G, genotyping 10 922 samples from four African populations. The nonsense allele was not associated with severe malaria (pooled allelic odds ratio 1.0; 95% confidence interval 0.89–1.12; P = 0.98). These results suggest a range of possible explanations including the existence of alternative selection pressures on CD36, co-evolution between host and parasite or confounding caused by allelic heterogeneity of CD36 deficiency.

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Frequency of human platelet antigens among blood donors in northeastern Thailand

Cited by 23 publications

References 14 publications

The human platelet alloantigen profile in blood donors from Amazonas, Brazil

The human platelet alloantigen profile in blood donors from Amazonas, Brazil

Platelet CD36 mediates interactions with endothelial cell–derived microparticles and contributes to thrombosis in mice

Positive selection of a CD36 nonsense variant in sub-Saharan Africa, but no association with severe malaria phenotypes

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