Data from: Platelet factor 4 and Duffy antigen required for platelet killing of Plasmodium falciparum

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.

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血小板通过与其感染的红细胞结合并杀死其中的寄生虫来限制间日疟原虫的生长。本研究揭示了血小板分子血小板因子4（PF4或CXCL4）和红细胞Duffy抗原受体（Fy）对于通过血小板介导的恶性疟原虫寄生虫的杀伤是必不可少的。PF4在血小板与感染红细胞接触时被释放，该蛋白质直接杀死红细胞内的寄生虫。PF4的这一功能对Fy的依赖性至关重要，Fy能够与PF4结合。Fy表达的遗传破坏抑制了PF4与感染细胞的结合，并随之防止了人血小板和重组人PF4对寄生虫的杀伤。因此，在Duffy阴性个体中，由于不表达Fy，血小板在疟疾感染期间提供的保护功能可能受到影响。