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Blood, 15 November 2005, Vol. 106, No. 10, pp. 3632-3638.
Prepublished online as a Blood First Edition Paper on July 26, 2005; DOI 10.1182/blood-2005-04-1574.
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Submitted April 18, 2005
Accepted July 13, 2005
Plasmodium falciparum rhoptry protein RSP2 triggers destruction of the erythroid lineage
Corinne Layez, Paulo Nogueira, Valery Combes, Fabio T Costa, Irene Juhan-Vague, Luiz H Pereira da Silva, and Jurg Gysin*
Unite de Parasitologie Experimentale URA Institut Pasteur/ Univ. Med. EA3282 IFR48, Faculte de Medecine, Universite de la Mediterranee, Marseille, France
Unidade de Imunologia E Parasitologia Experimental, CEPEM Centro de Pesquisa em Medicina Tropical, Porto Velho, Rondonia, Brazil
Departamento de Parasitologia, Universidade Estadual de Campinas, Campinas, Brazil
Laboratoire d'Hematologie, Faculte de Medecine, Universite de la Mediterranee, Marseille, France
* Corresponding author; email: gysin{at}medecine.univ-mrs.fr.
The destruction of erythrocytes and defects in erythropoiesis are among the most frequently observed cause of morbidity in severe falciparum malaria. The molecular mechanisms involved remain unclear, despite extensive investigation. We show here, for the first time, that tagging with the parasite rhoptry protein RSP-2 is not restricted to the surface of normal erythrocytes, as previously reported, but also extends to erythroid precursor cells in the bone marrow of anemic malaria patients.
Monoclonal mouse antibodies and human sera from patients with severe anemia, reacting with RSP2-tagged erythrocytes, induced cell destruction by phagocytosis and complement activation in vitro. Our observations reveal a new parasite mechanism implicated in the destruction of normal erythrocytes and probably dyserythropoiesis in malaria patients. These data suggest that the tagging of host cells with RSP-2 may trigger anemia in falciparum malaria.

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