The Fyx phenotype is associated with a missense mutation in the Fyb allele predicting Arg89Cys in the Duffy glycoprotein

Olsson, Martin L.; Smythe, Jonathan S.; Hansson, Carola; Poole, Joyce; Mallinson, Gary; Jones, Jeffrey W.; Avent, Neil D.; Daniels, Geoff

doi:10.1046/j.1365-2141.1998.01083.x

Cited by 88 publications

(111 citation statements)

References 32 publications

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“…(Tournamille et al 1998;Yazdanbakhsh et al 2000). Because the Fy x polymorphism results from a point mutation within the coding region of the Duffy gene, the nonerythroid cells should also show reduced expression and chemokine binding (Olsson et al 1998;Parasol et al 1998;Tournamille et al 1998;Wasniowska et al 2002).…”

Section: Discussionmentioning

confidence: 99%

“…ders erythrocytes Duffy-negative in the majority of African-Americans is a mutation occurring in the erythroidspecific promoter region and would not alter Duffy expression on nonerythroid cells (Olsson et al 1998;Peiper et al 1995;Tournamille et al 1995). Of the 34 specimens examined, three were Duffy-negative on erythrocytes but positive on vessels, and one was Duffynegative on erythrocytes with extremely low-level to no staining on vessels.…”

Section: Figurementioning

confidence: 99%

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Enhanced Expression of Duffy Antigen in the Lungs During Suppurative Pneumonia

Lee

Frevert

Thorning

et al. 2003

J Histochem Cytochem.

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S U M M A R YDuffy antigen is a chemokine binding protein expressed on the surface of erythrocytes and postcapillary venular endothelial cells. It binds selective CXC and CC chemokines with high affinity. Although Duffy antigen is present in the normal pulmonary vascular bed, it is not known whether its expression is altered by innate inflammatory responses in the lungs. We studied Duffy antigen expression by immunohistochemistry in autopsy lung specimens from 16 cases of suppurative pneumonia, 11 cases of acute lung injury, and seven normal lungs. In lungs with suppurative pneumonia, Duffy antigen was expressed in higher numbers of pre-and postcapillary parenchymal vessels compared to normal specimens or specimens with acute lung injury ( p Ͻ 0.03 and p Ͻ 0.02, respectively). Lungs with suppurative pneumonia also showed Duffy antigen expression on the alveolar septa, whereas this was a rare finding in normal specimens or in acute lung injury ( p Ͻ 0.02). Furthermore, Duffy antigen labeling of the alveolar septa localized to regions with airspace accumulation of neutrophil-rich exudates. In summary, Duffy antigen expression is increased in the vascular beds and alveolar septa of the lung parenchyma during suppurative pneumonia, suggesting that Duffy antigen may have a functional role in the lung parenchyma during inflammation.

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Section: Discussionmentioning

confidence: 99%

Section: Figurementioning

confidence: 99%

Enhanced Expression of Duffy Antigen in the Lungs During Suppurative Pneumonia

Lee

Frevert

Thorning

et al. 2003

J Histochem Cytochem.

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“…Patient A's sample was typed by serology as Fy (a-b-) which is very rare in Europeans but common in West Africans. 48 Subsequent molecular investigations, using allele-specific primers 49,50 and the blood group genotyping system BLOODchip, 42,51 demonstrated that patient A has the rare FY*0/FY*X genotype which predicts weakened Fy b antigen expression on erythrocytes. This weakened antigen expression, coupled with hemizygosity for the FY*B allele, made serological detection of the Fy b antigen very difficult and could have led to the erroneous interpretation that the Duffy antigen was diminished, as is the case in the 4.1R(-) mouse.…”

Section: Blood Group Antigen Expression On 41r(-) Erythrocytesmentioning

confidence: 99%

4.1R-deficient human red blood cells have altered phosphatidylserine exposure pathways and are deficient in CD44 and CD47 glycoproteins

Jeremy¹,

Plummer²,

Head³

et al. 2009

Haematologica

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BackgroundProtein 4.1R is an important component of the red cell membrane skeleton. It imparts structural integrity and has transmembrane signaling roles by direct interactions with transmembrane proteins and other membrane skeletal components, notably p55 and calmodulin. Design and MethodsSpontaneous and ligation-induced phosphatidylserine exposure on erythrocytes from two patients with 4.1R deficiency were studied, using CD47 glycoprotein and glycophorin C as ligands. We also looked for protein abnormalities in the 4.1R -based multiprotein complex. ResultsPhosphatidylserine exposure was significantly increased in 4.1R-deficient erythrocytes obtained from the two different individuals when ligands to CD47 glycoprotein were bound. Spontaneous phosphatidylserine exposure was normal. 4.1R, glycophorin C and p55 were missing or sharply reduced. Furthermore there was an alteration or deficiency of CD47 glycoprotein and a lack of CD44 glycoprotein. Based on a recent study in 4.1R-deficient mice, we found that there are clear functional differences between interactions of human red cell 4.1R and its murine counterpart. ConclusionsGlycophorin C is known to bind 4.1R, and we have defined previously that it also binds CD47. From our evidence, we suggest that 4.1R plays a role in the phosphatidylserine exposure signaling pathway that is of fundamental importance in red cell turnover. The linkage of CD44 to 4.1R may be relevant to this process. CD44 and CD47 glycoproteins. Haematologica 2009;94:1354-1361. doi:10.3324/haematol.2009 This is an open-access paper. 4.1R-deficient human red blood cells have altered phosphatidylserine exposure pathways and are deficient in CD44 and CD47 glycoproteins

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“…Erythrocyte Duffy negativity is explained by a single-nucleotide polymorphism (SNP) in a GATA-1 transcription factor binding site of the gene promoter (−33T → C) that governs erythroid expression (10). Variant antigens Fy a , Fy b , and Fy bweak are associated with SNPs in the gene's coding region (11)(12)(13)(14). Parallel studies identifying the P. vivax Duffy binding protein (PvDBP) (15)(16)(17) have provided the opportunity to dissect further the molecular interactions between parasite and host originally predicted by Miller (18,19).…”

mentioning

confidence: 99%

Plasmodium vivax clinical malaria is commonly observed in Duffy-negative Malagasy people

Ménard

Barnadas

Bouchier

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

346

354

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Malaria therapy, experimental, and epidemiological studies have shown that erythrocyte Duffy blood group-negative people, largely of African ancestry, are resistant to erythrocyte Plasmodium vivax infection. These findings established a paradigm that the Duffy antigen is required for P. vivax erythrocyte invasion. P. vivax is endemic in Madagascar, where admixture of Duffy-negative and Duffy-positive populations of diverse ethnic backgrounds has occurred over 2 millennia. There, we investigated susceptibility to P. vivax blood-stage infection and disease in association with Duffy blood group polymorphism. Duffy blood group genotyping identified 72% Duffy-negative individuals (FY*B ES /*B ES ) in community surveys conducted at eight sentinel sites. Flow cytometry and adsorption-elution results confirmed the absence of Duffy antigen expression on Duffy-negative erythrocytes. P. vivax PCR positivity was observed in 8.8% (42/476) of asymptomatic Duffy-negative people. Clinical vivax malaria was identified in Duffy-negative subjects with nine P. vivax monoinfections and eight mixed Plasmodium species infections that included P. vivax (4.9 and 4.4% of 183 participants, respectively). Microscopy examination of blood smears confirmed blood-stage development of P. vivax, including gametocytes. Genotyping of polymorphic surface and microsatellite markers suggested that multiple P. vivax strains were infecting Duffy-negative people. In Madagascar, P. vivax has broken through its dependence on the Duffy antigen for establishing human blood-stage infection and disease. Further studies are necessary to identify the parasite and host molecules that enable this Duffyindependent P. vivax invasion of human erythrocytes.erythrocyte | evolution | DARC | Madagascar

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The Fy^x phenotype is associated with a missense mutation in the Fy^b allele predicting Arg89Cys in the Duffy glycoprotein

Cited by 88 publications

References 32 publications

Enhanced Expression of Duffy Antigen in the Lungs During Suppurative Pneumonia

Enhanced Expression of Duffy Antigen in the Lungs During Suppurative Pneumonia

4.1R-deficient human red blood cells have altered phosphatidylserine exposure pathways and are deficient in CD44 and CD47 glycoproteins

Plasmodium vivax clinical malaria is commonly observed in Duffy-negative Malagasy people

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