ArticleMedical microbiology and immunology2014
Malarial anemia: digestive vacuole of Plasmodium falciparum mediates complement deposition on bystander cells to provoke hemophagocytosis.
Article in Medical microbiology and immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 30 citations in OpenAlex.
- Amino acid supplementation confers protection to red blood cells before Plasmodium falciparum bystander stress.Blood advances · 2024Article
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- One Haemolytic Anaemia May Hide Another: Paroxysmal Nocturnal Haemoglobinuria Masquerading AsEuropean journal of case reports in internal medicine · 2024Article
- Review
- Neutrophils activated by membrane attack complexes increase the permeability of melanoma blood vessels.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Host-parasite interactions duringFrontiers in immunology · 2022Review
- Beyond Binding: The Outcomes of Antibody-Dependent Complement Activation in Human Malaria.Frontiers in immunology · 2021Review
- Malaria, anemia, and invasive bacterial disease: A neutrophil problem?Journal of leukocyte biology · 2019Review
- Sticking for a Cause: The Falciparum Malaria Parasites Cytoadherence Paradigm.Frontiers in immunology · 2019Review
- Loss of complement regulatory proteins on uninfected erythrocytes in vivax and falciparum malaria anemia.JCI insight · 2018Article
- Analysis of erythrocyte dynamics in Rhesus macaque monkeys during infection with Plasmodium cynomolgi.Malaria journal · 2018Article
- Compstatin Cp40 blocks hematin-mediated deposition of C3b fragments on erythrocytes: Implications for treatment of malarial anemia.Clinical immunology (Orlando, Fla.) · 2016Article
- The Plasmodium falciparum blood stages acquire factor H family proteins to evade destruction by human complement.Cellular microbiology · 2016Article
- Severe falciparum malaria complicated by prolonged haemolysis and rhinomaxillary mucormycosis after parasite clearance: a case report.BMC infectious diseases · 2015Article
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Authors and funding
11 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The digestive vacuole (DV) of Plasmodium falciparum, which is released into the bloodstream upon rupture of each parasitized red blood cell (RBC), was recently discovered to activate the alternative complement pathway. In the present work, we show that C3- and C5-convertases assembling on the parasitic organelle are able to provoke deposition of activated C3 and C5b-9 on non-infected bystander erythrocytes. Direct contact of DVs with cells is mandatory for the effect, and bystander complement deposition occurs focally, possibly at the sites of contact. Complement opsonization promotes protracted erythrophagocytosis by human macrophages, an effect that is magnified when ring-stage infected RBCs with reduced CD55 and CD59, or paroxysmal nocturnal hemoglobinuria (PNH)-RBCs lacking these complement inhibitors are employed as targets. Bystander attack can also directly induce lysis of PNH-RBCs. Direct evidence for complement activation and bystander attack mediated by DVs was obtained through immunohistochemical analyses of brain paraffin sections from autopsies of patients who had died of cerebral malaria. C3d and the assembled C5b-9 complex could be detected in all sections, colocalizing with and often extending locally beyond massive accumulations of DVs that were identified under polarized light. This is the first demonstration that a complement-activating particle can mediate opsonization of bystander cells to promote their antibody-independent phagocytosis. The phenomenon may act in concert with other pathomechanisms to promote the development of anemia in patients with severe malaria.
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