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Plasmodium falciparum Uses gC1qR/HABP1/p32 as a Receptor to Bind to Vascular Endothelium
 

Summary: Plasmodium falciparum Uses gC1qR/HABP1/p32
as a Receptor to Bind to Vascular Endothelium
and for Platelet-Mediated Clumping
Anup Kumar Biswas1,2¤
, Abdul Hafiz1
, Bhaswati Banerjee2
, Kwang Sik Kim3
, Kasturi Datta2*
, Chetan E. Chitnis1*
1 Malaria Group, International Centre for Genetic Engineering and Biotechnology, New Delhi, India, 2 School of Environmental Sciences, Jawaharlal Nehru University, New
Delhi, India, 3 Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America
The ability of Plasmodium falciparum­infected red blood cells (IRBCs) to bind to vascular endothelium, thus enabling
sequestration in vital host organs, is an important pathogenic mechanism in malaria. Adhesion of P. falciparum IRBCs
to platelets, which results in the formation of IRBC clumps, is another cytoadherence phenomenon that is associated
with severe disease. Here, we have used in vitro cytoadherence assays to demonstrate, to our knowledge for the first
time, that P. falciparum IRBCs use the 32-kDa human protein gC1qR/HABP1/p32 as a receptor to bind to human brain
microvascular endothelial cells. In addition, we show that P. falciparum IRBCs can also bind to gC1qR/HABP1/p32 on
platelets to form clumps. Our study has thus identified a novel host receptor that is used for both adhesion to vascular
endothelium and platelet-mediated clumping. Given the association of adhesion to vascular endothelium and platelet-
mediated clumping with severe disease, adhesion to gC1qR/HABP1/p32 by P. falciparum IRBCs may play an important

  

Source: Arnold, Jonathan - Nanoscale Science and Engineering Center & Department of Genetics, University of Georgia

 

Collections: Biotechnology