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.

血小板可通过结合疟原虫感染的红细胞并在胞内杀灭疟原虫，从而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或CXCL4）与红细胞达菲抗原受体（erythrocyte Duffy-antigen receptor，Fy）是血小板介导杀灭恶性疟原虫（Plasmodium falciparum）所必需的分子。当血小板与疟原虫感染的红细胞接触时，会释放PF4，该蛋白可直接杀灭红细胞内的疟原虫。PF4的这一功能严格依赖于能够结合PF4的Fy受体。敲除Fy的表达会抑制PF4与感染红细胞的结合，同时阻断人类血小板与重组人PF4对疟原虫的杀灭作用。因此，在不表达Fy的达菲阴性个体中，血小板在疟疾感染过程中所提供的保护功能可能会受到削弱。