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Data from: Platelet factor 4 and Duffy antigen required for platelet killing of Plasmodium falciparum
datasetposted on 2022-06-10, 03:03 authored by Brendan J. McMorran, Laura Wieczorski, Karen E. Drysdale, Jo-Anne Chan, Hong Ming Huang, Clare Smith, Chalachew Mitiku, James G. Beeson, Gaetan Burgio, Simon J. Foote
Platelets restrict the growth of intraerythrocytic malaria parasites by binding to parasitized cells and killing the parasite within. Here, we show that the platelet molecule platelet factor 4 (PF4 or CXCL4) and the erythrocyte Duffy-antigen receptor (Fy) are necessary for platelet-mediated killing of Plasmodium falciparum parasites. PF4 is released by platelets on contact with parasitized red cells, and the protein directly kills intraerythrocytic parasites. This function for PF4 is critically dependent on Fy, which binds PF4. Genetic disruption of Fy expression inhibits binding of PF4 to parasitized cells and concomitantly prevents parasite killing by both human platelets and recombinant human PF4. The protective function afforded by platelets during a malarial infection may therefore be compromised in Duffy-negative individuals, who do not express Fy.
Usage NotesMcMorran Figure 1McMorran Figure 2McMorran Figure 3McMorran Figure 4McMorran Figure S1McMorran Figure S3McMorran Figure S4McMorran Figure S5McMorran Figure S7McMorran Figure S8
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