Adhesion of normal and Plasmodium falciparum ring–infected erythrocytes to endothelial cells and the placenta involves the rhoptry-derived ring surface protein-2
2003; Elsevier BV; Volume: 101; Issue: 12 Linguagem: Inglês
10.1182/blood-2002-12-3710
ISSN1528-0020
AutoresJean-Bernard Lekana Douki, Yvon Sterkers, Catherine Lépolard, Boubacar Traoré, Fábio Trindade Maranhão Costa, Artur Scherf, Jürg Gysin,
Tópico(s)Complement system in diseases
ResumoAbstract Recent findings have challenged the current view of Plasmodium falciparum (P falciparum) blood-stage biology by demonstrating the cytoadhesion of early ring-stage–infected erythrocytes (rIEs) to host endothelial cells and placental syncytiotrophoblasts. The adhesion of rIEs was observed only in parasites that bind to the placenta via chondroitin sulfate A (CSA). In this work, a panel of mouse monoclonal antibodies (mAbs) that specifically inhibit cytoadhesion of rIEs but not of mature IEs was generated The previously described ring surface protein 2 (RSP-2), a 42-kDa protein, was identified as the target of the ring-stage–specific mAbs. Time course surface fluorescence experiments revealed a short overlap (approximately 4 hours) of expression between RSP-2 and P falciparum erythrocyte membrane protein 1 (PfEMP1). Their consecutive expression enables IEs to adhere to endothelial cells during the entire blood-stage cycle. During this study, a new phenotype was detected in parasite cultures, the adhesion of normal erythrocytes (nEs) to endothelial cells. All adherent nEs were coated with RSP-2. Immunolocalization studies show that RSP-2 is a rhoptry-derived protein that is discharged onto the erythrocyte membrane during contact with merozoites. Our results identify RSP-2 as a key molecule in sequestration of young blood-stage forms and nEs to endothelial cells.
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