ArticleBlood2011
Plasmodium falciparum uses a key functional site in complement receptor type-1 for invasion of human erythrocytes.
Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 54 citations in OpenAlex.
- Deposition of complement regulators on the surface of Plasmodium falciparum merozoites depends on the immune status of the host.PLoS pathogens · 2025Article
- Determining Ligand Binding and Specificity Within the βBiomolecules · 2025Article
- A novel and rapid method to purify the human complement opsonin C3b from human plasma.Frontiers in immunology · 2025Article
- Triple-fusion protein (TriFu): A potent, targeted, enzyme-like inhibitor of all three complement activation pathways.The Journal of biological chemistry · 2024Article
- Complement receptor 1 is the human erythrocyte receptor forProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Population-specific positive selection on low CR1 expression in malaria-endemic regions.PloS one · 2023Article
- Review
- The Cellular and Molecular Interaction Between Erythrocytes andFrontiers in cellular and infection microbiology · 2022Review
- Few Plasmodium falciparum merozoite ligand and erythrocyte receptor pairs show evidence of balancing selection.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2019Article
- Transferrin receptor 1 is a reticulocyte-specific receptor forScience (New York, N.Y.) · 2018Article
- No Evidence that Knops Blood Group Polymorphisms Affect Complement Receptor 1 Clustering on Erythrocytes.Scientific reports · 2017Article
- Protection of host cells by complement regulators.Immunological reviews · 2016Review
- The association between naturally acquired IgG subclass specific antibodies to the PfRH5 invasion complex and protection from Plasmodium falciparum malaria.Scientific reports · 2016Article
- Merozoite surface proteins in red blood cell invasion, immunity and vaccines against malaria.FEMS microbiology reviews · 2016Review
- Red cell receptors as access points for malaria infection.Current opinion in hematology · 2016Review
- Red blood cell complement receptor one level varies with Knops blood group, α(+)thalassaemia and age among Kenyan children.Genes and immunity · 2016Article
- The Plasmodium falciparum blood stages acquire factor H family proteins to evade destruction by human complement.Cellular microbiology · 2016Article
- Plasmodium falciparum Adhesins Play an Essential Role in Signalling and Activation of Invasion into Human Erythrocytes.PLoS pathogens · 2015Article
- Characterization of Inhibitors and Monoclonal Antibodies That Modulate the Interaction between Plasmodium falciparum Adhesin PfRh4 with Its Erythrocyte Receptor Complement Receptor 1.The Journal of biological chemistry · 2015Article
- Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 4 countries.
Funding
Abstract
The Plasmodium falciparum adhesin PfRh4 binds to complement receptor type-1 (CR1) on human erythrocytes and mediates a glycophorin-independent invasion pathway. CR1 is a complement regulator and immune-adherence receptor on erythrocytes required for shuttling of C3b/C4b-opsonized particles to liver and spleen for phagocytosis. Using recombinant CR1 constructs, we mapped the recognition site for PfRh4 to complement control protein modules 1 to 3 (CCP1-3) at the membrane-distal amino terminus of CR1. This region of CR1 binds to C4b and C3b and accelerates decay of both classic pathway and alternative pathway C3 and C5 convertases. CCP1-3 competed for PfRh4 binding to erythroid CR1 and inhibited the PfRh4-CR1 invasion pathways across a wide range of P falciparum strains. PfRh4 did not bind significantly to other CR1 constructs, including CCP15-17, which is 85% identical to CCP1-3. PfRh4 binding to CR1 did not affect its C3b/C4b binding capability, and we show evidence for a ternary complex between CCP1-3, C4b, and PfRh4. PfRh4 binding specifically inhibited CR1's convertase decay-accelerating activity, whereas there was no effect on factor H-mediated decay-accelerating activity. These results increase our understanding of the functional implications of CR1 engagement with PfRh4 and highlight the interplay between complement regulation and infection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.