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The levels of CD16/Fc gamma receptor III A on CD14+CD16+ monocytes are higher in children with severe Plasmodium falciparum anemia than in children with cerebral or uncomplicated malaria

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  • 1,
  • 1,
  • 2,
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Malaria Journal20109 (Suppl 2) :P29

  • Published:


  • Malaria
  • Tumor Necrosis Factor Alpha
  • Plasmodium Falciparum
  • Necrosis Factor Alpha
  • Malaria Control


Fc gamma receptor IIIA (CD16/FCγRIIIA) on monocytes/macro-phages may play an important role in the pathogenesis of severe malarial anemia (SMA) by promoting phagocytosis of IgG-coated uninfected red cells and by allowing the production of tumor necrosis factor alpha (TNF-α) upon cross-linking by immune complexes (ICs). However, not much is known about the differential expression of this receptor on monocytes of children with severe malaria and uncomplicated malaria.

Materials and methods

We investigated the expression of CD16/FCγRIIIA on monocytes of children with SMA, cerebral malaria (CM), and their age-matched uncomplicated malaria controls by flow cytometry. Since CD14low (CD14+) monocytes are considered more mature and macrophage-like than CD14high (CD14++) monocytes, we also compared the level of expression of CD16/FCγRIIIA according to the CD14 level and studied the relationship between CD16/FCγRIIIA expression and intracellular TNF- production upon stimulation by ICs.


CD16/FcγRIIIA expression was the highest overall on CD14+CD16+ monocytes of children with SMA at enrollment. At convalescence, SMA children were the only ones to show a significant decline in the same parameter. In contrast, there were no significant differences among groups in the expression of CD16/FCγRIIIA on CD14++CD16+ monocytes. A greater percentage of CD14+CD16+ monocytes produced TNF-α upon stimulation than any other monocyte subset, and the amount of intracellular TNF-α correlated positively with CD16/FcRIIIA expression. Furthermore, there was an inverse correlation between hemoglobin levels and CD16/FCγRIIIA expression in children with SMA and their controls.


These data suggest that monocytes of children with SMA respond differently to Plasmodium falciparum infection by overexpressing CD16/FCγRIIIA as they mature, which could enhance erythrophagocytosis and TNF production.

Authors’ Affiliations

Department of Pre-clinical sciences, Kenyatta University, Nairobi, Kenya
US Army Medical Research Unit and the Kenya Medical Research Institute, Nairobi, Kenya
Department of Medicine, Division of Infectious Diseases, and Department of Microbiology and Immunology, the Pennsylvania State University College of Medicine, Hershey, PA, USA


  1. Waitumbi JN, Opollo MO, Muga RO, Misore AO, Stoute JA: Red cell surface changes and erythrophagocytosis in children with severe Plasmodium falciparum anemia. Blood. 2000, 95: 1481-1486.PubMedGoogle Scholar
  2. Ravetch JV, Bolland S: IgG Fc receptors. Annu Rev Immunol. 2001, 19: 275-290. 10.1146/annurev.immunol.19.1.275.View ArticlePubMedGoogle Scholar


© Stoute et al; licensee BioMed Central Ltd. 2010

This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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