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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. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-11-3820v1 104/10/3364    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Ayi, K. Articles by Arese, P. Search for Related Content PubMed PubMed Citation Articles by Ayi, K. Articles by Arese, P. Related Collections Phagocytes Red Cells Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  RED CELLS 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 From the Dipartimento di Genetica, Biologia, e Biochimica and the Dipartimento di Discipline Pediatriche, Università di Torino, Torino, Italy. High frequency of erythrocyte (red blood cell [RBC]) genetic disorders such as sickle cell trait, thalassemia trait, homozygous hemoglobin C (Hb-C), and glucose-6-phosphate dehydrogenase (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 RBCs. We suggested enhanced phagocytosis of rings, the early intraerythrocytic form of the parasite, as an alternative explanation for protection in G6PD deficiency. We show here that P falciparum developed similarly in normal RBCs and in sickle trait, beta- and alpha-thalassemia trait, and HbH RBCs. We also show that membrane-bound hemichromes, autologous immunoglobulin G (IgG) and complement C3c fragments, aggregated band 3, and phagocytosis by human monocytes were remarkably higher in rings developing in all mutant RBCs considered except alpha-thalassemia trait. Phagocytosis of ring-parasitized mutant RBCs was predominantly complement mediated and very similar to phagocytosis of senescent or damaged normal RBCs. Trophozoite-parasitized normal and mutant RBCs were phagocytosed similarly in all conditions examined. Enhanced phagocytosis of ring-parasitized mutant RBCs may represent the common mechanism for malaria protection in nonimmune individuals affected by widespread RBC mutations, while individuals with alpha-thalassemia trait are likely protected by a different mechanism. (Blood. 2004;104:3364-3371) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: P. M. Durand and T. L. Coetzer Hereditary red cell disorders and malaria resistance Haematologica, July 1, 2008; 93(7): 961 - 963. [Full Text] [PDF] A. Enevold, J. P. Lusingu, B. Mmbando, M. Alifrangis, M. M. Lemnge, I. C. Bygbjerg, T. G. Theander, and L. S. Vestergaard Reduced Risk of Uncomplicated Malaria Episodes in Children with Alpha+-Thalassemia in Northeastern Tanzania Am J Trop Med Hyg, May 1, 2008; 78(5): 714 - 720. [Abstract] [Full Text] [PDF] K. Ayi, G. Min-Oo, L. Serghides, M. Crockett, M. Kirby-Allen, I. Quirt, P. Gros, and K. C. 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