Science 

IMMUNOLOGY

Platelets Kill the Parasite Within

1. Christian R. Engwerda1, 
2. Michael F. Good2

+Author Affiliations

1. ¹Queensland Institute of Medical Research, Brisbane, QLD Australia.
2. ²Institute for Glycomics, Griffith University, Gold Coast, QLD Australia.

1. E-mail: michael.good@griffith.edu.au

The estimated 216 million cases of malaria in 2010 resulted in about 655,000 deaths, around 86% of which were children under the age of 5 (1), mainly in sub-Saharan Africa. Most of these deaths are caused by the protozoan parasite Plasmodium falciparum. Our poor understanding of innate resistance and the development of immunity to P. falciparum is an obstacle to developing vaccines and new therapeutics. The human body has numerous defenses to protect itself against severe forms of malaria. One such strategy, previously underappreciated, involves platelets—unnucleated fragments of megakaryocytes normally thought of as being critical solely to prevent hemorrhage. On page 1348 in this issue, McMorran et al. (2) reveal a mechanism by which platelets can recognize infected red blood cells and kill the parasite within (see the figure)

Destroying P. falciparum.

(A) Activated platelets containing PF4-laden granules bind to parasitized red blood cells that express the Duffy-antigen receptor. (B) Upon binding [through CD36 on platelets and a parasite receptor on the red blood cell, possibly P. falciparum erythrocyte membrane protein 1 (PfEMP-1) (15)], PF4 is released and binds to the Duffy-antigen receptor on red blood cells. (C) The PF4–Duffy-antigen receptor complex translocates into the cell, colocalizes with intracellular parasites, and then kills the parasites.

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