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Blood, 15 November 2004, Vol. 104, No. 10, pp. 3364-3371.
Prepublished online as a Blood First Edition Paper on July 27, 2004; DOI 10.1182/blood-2003-11-3820.
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Submitted November 13, 2003
Accepted May 25, 2004
Enhanced phagocytosis of ring-parasitized mutant erythrocytes. A common mechanism that may explain protection against falciparum-malaria in sickle-trait and beta-thalassemia-trait
Kodjo Ayi, Franco Turrini, Antonio Piga, and Paolo Arese*
Dipartimento di Genetica, Biologia, Biochimica, Universita di Torino, Torino, Italy
Dipartimento di Discipline Pediatriche, Universita di Torino, Torino, Italy
* Corresponding author; email: paolo.arese{at}unito.it.
High frequency of erythrocyte (RBC) genetic disorders such as sickle-cell trait, thalassemia-trait, homozygous Hb-C and G6PD-deficiency in regions with high incidence of Plasmodium falciparum malaria, and case-control studies support the protective role of those conditions. Protection has been attributed to defective parasite growth or to enhanced removal of the parasitized RBC. We suggested enhanced phagocytosis of rings, the early intraerythrocytic form of the parasite, as an alternative explanation for protection in G6PD-deficiency (Cappadoro et al. Blood. 1998;92:2527-2534). We show here that P falciparum developed similarly in normal RBC and in sickle-trait, beta- and alpha-thalassemia trait, and HbH RBC. We also show that membrane-bound hemichromes, autologous IgG and complement C3c fragments, aggregated band-3 and phagocytosis by human monocytes were remarkably higher in rings developing in all above mutant RBC except alpha-thalassemia trait. Phagocytosis of ring-parasitized mutant RBC was predominantly complement-mediated and very similar to phagocytosis of senescent or damaged normal RBC. Trophozoite-parasitized normal and mutant RBC were phagocytosed similarly in all conditions examined. Enhanced phagocytosis of ring-parasitized mutant RBC may represent the common mechanism for malaria protection in non-immune individuals affected by widespread RBC mutations, while individuals with alpha-thalassemia trait are likely protected by a different mechanism.
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