ArticleMolecular medicine (Cambridge, Mass.)
Reduced immune complex binding capacity and increased complement susceptibility of red cells from children with severe malaria-associated anemia.
Article in Molecular medicine (Cambridge, Mass.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 51 citations in OpenAlex.
- Targeting mucosal immunity in malaria control: the underexplored role of IgA.Frontiers in malaria · 2025Article
- Inhibition of Complement Will Substantially Reduce the Anemia of Malaria.Journal of immunology research · 2025Review
- Xanthine oxidase levels and immune dysregulation are independently associated with anemia in Plasmodium falciparum malaria.Scientific reports · 2023Article
- Complement component 3 mutations alter the longitudinal risk of pediatric malaria and severe malarial anemia.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- Beyond Binding: The Outcomes of Antibody-Dependent Complement Activation in Human Malaria.Frontiers in immunology · 2021Review
- Comediation of Erythrocyte Haemolysis by Erythrocyte-Derived Microparticles and Complement during Malaria Infection.Advances in hematology · 2020Article
- Loss of complement regulatory proteins on uninfected erythrocytes in vivax and falciparum malaria anemia.JCI insight · 2018Article
- Red blood cell complement receptor one level varies with Knops blood group, α(+)thalassaemia and age among Kenyan children.Genes and immunity · 2016Article
- Potential immune mechanisms associated with anemia in Plasmodium vivax malaria: a puzzling question.Infection and immunity · 2014Review
- Functions of Antibodies.Microbiology spectrum · 2014Article
- Article
- Plasmodium coatneyi in rhesus macaques replicates the multisystemic dysfunction of severe malaria in humans.Infection and immunity · 2013Article
- Malaria inhibits surface expression of complement receptor 1 in monocytes/macrophages, causing decreased immune complex internalization.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Sequential Plasmodium chabaudi and Plasmodium berghei infections provide a novel model of severe malarial anemia.Infection and immunity · 2012Article
- Early and extensive CD55 loss from red blood cells supports a causal role in malarial anaemia.Malaria journal · 2011Article
- Dual role of erythrocyte complement receptor type 1 in immune complex-mediated macrophage stimulation: implications for the pathogenesis of Plasmodium falciparum malaria.Clinical and experimental immunology · 2011Article
- The levels of CD16/Fc gamma receptor IIIA on CD14+ CD16+ monocytes are higher in children with severe Plasmodium falciparum anemia than in children with cerebral or uncomplicated malaria.Infection and immunity · 2010Article
- Hemolysis is associated with low reticulocyte production index and predicts blood transfusion in severe malarial anemia.PloS one · 2010Article
- Blood groups and malaria: fresh insights into pathogenesis and identification of targets for intervention.Current opinion in hematology · 2009Review
- Rate of red blood cell destruction varies in different strains of mice infected with Plasmodium berghei-ANKA after chronic exposure.Malaria journal · 2009Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Plasmodium falciparum malaria causes 1-2 million deaths per year. Most deaths occur as a result of complications such as severe anemia and cerebral malaria (CM) (coma). Red cells of children with severe malaria-associated anemia (SMA) have acquired deficiencies in the complement regulatory proteins complement receptor 1 (CR1, CD35) and decay accelerating factor (DAF, CD55). We investigated whether these deficiencies affect the ability of erythrocytes to bind immune complexes (ICs) and regulate complement activation. We recruited 75 children with SMA (Hb < or = 6 g/dL) from the holoendemic malaria region of the Lake Victoria basin, western Kenya, and 74 age- and gender-matched uncomplicated malaria controls. In addition, we recruited 32 children with CM and 52 age- and gender-matched controls. Deficiencies in red cell CR1 and CD55 in children with SMA were accompanied by a marked decline in IC binding capacity and increased C3b deposition in vivo and ex vivo. Importantly, these changes were specific because they were not seen in red cells of children with CM or their controls. These data suggest that the declines in red cell CR1 and CD55 seen in children with SMA are of physiologic significance and may predispose erythrocytes to complement-mediated damage and phagocytosis in vivo.
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Registered trials
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