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.

血小板可通过结合被寄生虫感染的细胞并杀灭胞内寄生虫，抑制红细胞内疟原虫的增殖。本研究证实，血小板因子4（platelet factor 4, PF4/CXCL4）与红细胞达菲抗原受体（Duffy-antigen receptor, Fy）是血小板介导杀灭恶性疟原虫（Plasmodium falciparum）的必需分子。血小板在接触被寄生虫感染的红细胞时会释放PF4，该蛋白可直接杀灭红细胞内的疟原虫。PF4的上述功能完全依赖于能够结合PF4的Fy。若通过基因手段阻断Fy的表达，会抑制PF4与被感染细胞的结合，同时也会使人血小板与重组人PF4均无法杀灭疟原虫。因此，在不表达Fy的达菲阴性个体中，疟疾感染期间血小板所提供的保护作用可能会受到削弱。