Discovery of the Expected Hæmagglutinin, Anti-Fyb

Ikin, Elizabeth W.; Mourant, A. E.; Pettenkofer, H. J.; Blumenthal, G.

doi:10.1038/1681077b0

Cited by 80 publications

(27 citation statements)

References 2 publications

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“…The expected Fy b antisera was discovered in Berlin shortly thereafter (Ikin et al, 1951); surveys of European populations suggested frequencies for the co-dominantly expressed Fy a and Fy b antigens of 35% and 65%, respectively (Cutbush et al, 1950; Ikin et al, 1951). Upon screening, a series of blood samples from African-American donors to the Knickerbocker Blood Bank of New York City, Sanger et al observed that 68% of the samples did not react with either the Fy a or Fy b antisera (Sanger et al, 1955).…”

Section: Resistance To P Vivax and Insights On Malaria Red Cell Imentioning

confidence: 99%

Red Blood Cell Polymorphism and Susceptibility to Plasmodium vivax

Zimmerman

Ferreira

Howes

et al. 2013

Advances in Parasitology

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Resistance to Plasmodium vivax blood-stage infection has been widely recognised to result from absence of the Duffy (Fy) blood group from the surface of red blood cells (RBCs) in individuals of African descent. Interestingly, recent studies from different malaria-endemic regions have begun to reveal new perspectives on the association between Duffy gene polymorphism and P. vivax malaria. In Papua New Guinea and the Americas, heterozygous carriers of a Duffy-negative allele are less susceptible to P. vivax infection than Duffy-positive homozygotes. In Brazil, studies show that the Fya antigen, compared to Fyb, is associated with lower binding to the P. vivax Duffy-binding protein and reduced susceptibility to vivax malaria. Additionally, it is interesting that numerous studies have now shown that P. vivax can infect RBCs and cause clinical disease in Duffy-negative people. This suggests that the relationship between P. vivax and the Duffy antigen is more complex than customarily described. Evidence of P. vivax Duffy-independent red cell invasion indicates that the parasite must be evolving alternative red cell invasion pathways. In this chapter, we review the evidence for P. vivax Duffy-dependent and Duffy-independent red cell invasion. We also consider the influence of further host gene polymorphism associated with malaria endemicity on susceptibility to vivax malaria. The interaction between the parasite and the RBC has significant potential to influence the effectiveness of P. vivax-specific vaccines and drug treatments. Ultimately, the relationships between red cell polymorphisms and P. vivax blood-stage infection will influence our estimates on the population at risk and efforts to eliminate vivax malaria.

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Section: Resistance To P Vivax and Insights On Malaria Red Cell Imentioning

confidence: 99%

Red Blood Cell Polymorphism and Susceptibility to Plasmodium vivax

Zimmerman

Ferreira

Howes

et al. 2013

Advances in Parasitology

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“…An antibody termed anti-Fy a present in the plasma of a polytransfused hemophiliac, Mr. Duffy, was found to cause a delayed hemolytic transfusion reaction. In the following year, an antibody to the antithetic antigen, Fy b , was found in a multigravida exposed to fetal Fy b erythrocytes (Ikin et al, 1951). Subsequently, three “Duffy-positive” phenotypes were described: Fy(a+b–), Fy(a–b+), and Fy(a+b+), arising from combinations of the antithetical co-dominant FYA and FYB genes (Klein and Anstee, 2005).…”

Section: Duffy Blood Group Antigenmentioning

confidence: 99%

Duffy antigen receptor for chemokines and its involvement in patterning and control of inflammatory chemokines

Novitzky‐Basso

Rot

2012

Front. Immun.

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Leukocyte functions are linked to their migratory responses, which, in turn, are largely determined by the expression profile of classical chemokine receptors. Upon binding their cognate chemokines, these G-protein-coupled receptors (GPCRs) initiate signaling cascades and downstream molecular and cellular responses, including integrin activation and cell locomotion. Chemokines also bind to an alternative subset of chemokine receptors, which have serpentine structure characteristic for GPCRs but lack DRYLAIV consensus motive required for coupling to G-proteins. Duffy antigen receptor for chemokines (DARC) is a member of this atypical receptor subfamily. DARC binds a broad range of inflammatory CXC and CC chemokines and is expressed by erythrocytes, venular endothelial cells, and cerebellar neurons. Erythrocyte DARC serves as blood reservoir of cognate chemokines but also as a chemokine sink, buffering potential surges in plasma chemokine levels. Endothelial cell DARC internalizes chemokines on the basolateral cell surface resulting in subsequent transcytosis of chemokines and their immobilization on the tips of apical microvilli. These DARC-mediated endothelial cell interactions allow chemokines produced in the extravascular tissues to optimally function as arrest chemokines on the luminal endothelial cell surface.

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“…A second antithetic antigen Fyb [2] was shortly after discovered. In 1955, it was shown that antigens of Duffy blood group system were missing in red blood cells (named Fy(a-b-)) from a large proportion of West African ascent population (RBC-WAAP) [3].…”

Section: Darcmentioning

confidence: 99%