Platelet Factor 4 and Duffy Antigen Required for Platelet Killing of Plasmodium falciparum

@article{McMorran2012PlateletF4,
  title={Platelet Factor 4 and Duffy Antigen Required for Platelet Killing of Plasmodium falciparum},
  author={B. McMorran and Laura Wieczorski and K. Drysdale and J. Chan and H. Huang and Clare M. Smith and Chalachew Mitiku and J. Beeson and G. Burgio and S. Foote},
  journal={Science},
  year={2012},
  volume={338},
  pages={1348 - 1351}
}
Platelets Poison Parasites Activated platelets bound to malaria parasite–infected red blood cells were once thought to contribute to pathogenesis, but recently the platelets have been found to have a protective effect. McMorran et al. (p. 1348; see the Perspective by Engwerda and Good) extended this discovery to show that platelet activation releases intracellular granules containing a chemokine, PF4, which is internalized by Plasmodium falciparum–infected red cells. Subsequently, mature… Expand
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References

SHOWING 1-10 OF 39 REFERENCES
Identification of a platelet membrane glycoprotein as a falciparum malaria sequestration receptor.
TLDR
The portion of the CD36 molecule that reverses cytoadherence may be useful therapeutically for rapid reversal of sequestration in cerebral malaria. Expand
Platelets Kill Intraerythrocytic Malarial Parasites and Mediate Survival to Infection
TLDR
Results indicate a protective function for platelets in the early stages of erythrocytic infection distinct from their role in cerebral malaria. Expand
Platelet-mediated clumping of Plasmodium falciparum-infected erythrocytes is a common adhesive phenotype and is associated with severe malaria.
  • A. Pain, D. Ferguson, +4 authors D. Roberts
  • Biology, Medicine
  • Proceedings of the National Academy of Sciences of the United States of America
  • 2001
TLDR
It is established that platelet-mediated clumping is strongly associated with severe malaria and Precise definition of the molecular basis of this intriguing adhesive phenotype may help to elucidate the complex pathophysiology of malaria. Expand
Plasmodium falciparum growth inhibition by human platelets in vitro.
TLDR
The results show that platelets induce a dose-related growth inhibition of P. falciparum, at least in vitro, although the importance of their role played in vivo in malarial immunity has yet to be evaluated. Expand
Platelet factor 4 mediates inflammation in experimental cerebral malaria.
TLDR
It is concluded that Plasmodium-infected RBCs can directly activate platelets, and platelet-derived PF4 then contributes to immune activation and T cell trafficking as part of the pathogenesis of ECM. Expand
Expression of the Duffy antigen in K562 cells. Evidence that it is the human erythrocyte chemokine receptor.
TLDR
Transfection of the Duffy blood group antigen into a human erythroleukemic cell line and covalent incorporation of radiolabeled MGSA into a protein of molecular mass 47 kDa and cross-linking was inhibited in the presence of unlabeling MGSA provide evidence that the DuffyBlood group antigen is the same protein as thehuman erythrocyte chemokine receptor. Expand
Duffy antigen is important for the lethal effect of the lethal strain of Plasmodium yoelii 17XL
TLDR
Parasitemia increased exponentially after infection with Plasmodium berghei NK65, P. chabaudi, and P. vinckei in Duffy antigen knockout, glycophorin A knockout, and wild-type mice, indicating that the Duffy antigen and glycopharin A are not essential for these malaria parasites. Expand
Platelet-induced autoagglutination of Plasmodium falciparum-infected red blood cells and disease severity in Thailand.
TLDR
In multivariate analyses, high parasitemia and cerebral malaria were associated independently with parasite agglutination. Expand
Vacuolar uptake of host components, and a role for cholesterol and sphingomyelin in malarial infection
TLDR
Novel mechanisms regulated by the DRM lipids, sphingomyelin and cholesterol, mediate the uptake of host DRM proteins and maintenance of the intracellular vacuole in the non‐endocytic red cell, which may have implications for intrACEllular parasitism and pathogenesis. Expand
Platelet Factor 4: Production, Structure, and Physiologic and Immunologic Action
  • M. B. Zucker, I. Katz
  • Biology, Medicine
  • Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine
  • 1991
TLDR
Thrombospondin, platelet-derived growth factor, and compounds derived from platelet basic protein such as β-thromboglobulin (β-TG) are found in platelet α-granules in addition to PF4 and all are secreted when platelets are appropriately stimulated. Expand
...
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3
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