ArticlePLoS pathogens2010
Complement receptor 1 is a sialic acid-independent erythrocyte receptor of Plasmodium falciparum.
Article in PLoS pathogens, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 97 citations in OpenAlex.
- Nanobodies against Plasmodium adhesins that block receptor engagement and malaria parasite invasion.The Biochemical journal · 2026Article
- Invasion preferences suggest a possible role for Plasmodium falciparum parasites in the expansion of Duffy negativity in West and Central Africa.Molecular biology and evolution · 2026Article
- Review
- Complement receptor 1 is the human erythrocyte receptor forProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Microwaves can kill malaria parasites non-thermally.Frontiers in cellular and infection microbiology · 2023Article
- Deceiving and escaping complement - the evasive journey of the malaria parasite.Trends in parasitology · 2022Review
- Review
- Phenotypic characterization of GhanaianFrontiers in immunology · 2022Article
- Erythrocyte CD55 mediates the internalization ofeLife · 2021Article
- Blood donor variability is a modulatory factor for P. falciparum invasion phenotyping assays.Scientific reports · 2021Article
- Interaction Between the Complement System and Infectious Agents - A Potential Mechanistic Link to Neurodegeneration and Dementia.Frontiers in cellular neuroscience · 2021Review
- Antiplasmodial activity ofJournal of parasitic diseases : official organ of the Indian Society for Parasitology · 2020Article
- The Putative TCP-1 Chaperonin Is an Important Player Involved in Sialic Acid-Dependent Host Cell Invasion byFrontiers in microbiology · 2020Article
- Complement Receptor 1 availability on red blood cell surface modulates Plasmodium vivax invasion of human reticulocytes.Scientific reports · 2019Article
- Article
- A forward genetic screen reveals a primary role for Plasmodium falciparum Reticulocyte Binding Protein Homologue 2a and 2b in determining alternative erythrocyte invasion pathways.PLoS pathogens · 2018Article
- Functional Characterization of Plasmodium falciparum Surface-Related Antigen as a Potential Blood-Stage Vaccine Target.The Journal of infectious diseases · 2018Article
- Two complement receptor one alleles have opposing associations with cerebral malaria and interact with αeLife · 2018Article
- Plasmodium falciparum strains spontaneously switch invasion phenotype in suspension culture.Scientific reports · 2018Article
- Beyond Hemoglobin: Screening for Malaria Host Factors.Trends in genetics : TIG · 2018Review
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
Plasmodium falciparum is a highly lethal malaria parasite of humans. A major portion of its life cycle is dedicated to invading and multiplying inside erythrocytes. The molecular mechanisms of erythrocyte invasion are incompletely understood. P. falciparum depends heavily on sialic acid present on glycophorins to invade erythrocytes. However, a significant proportion of laboratory and field isolates are also able to invade erythrocytes in a sialic acid-independent manner. The identity of the erythrocyte sialic acid-independent receptor has been a mystery for decades. We report here that the complement receptor 1 (CR1) is a sialic acid-independent receptor for the invasion of erythrocytes by P. falciparum. We show that soluble CR1 (sCR1) as well as polyclonal and monoclonal antibodies against CR1 inhibit sialic acid-independent invasion in a variety of laboratory strains and wild isolates, and that merozoites interact directly with CR1 on the erythrocyte surface and with sCR1-coated microspheres. Also, the invasion of neuraminidase-treated erythrocytes correlates with the level of CR1 expression. Finally, both sialic acid-independent and dependent strains invade CR1 transgenic mouse erythrocytes preferentially over wild-type erythrocytes but invasion by the latter is more sensitive to neuraminidase. These results suggest that both sialic acid-dependent and independent strains interact with CR1 in the normal red cell during the invasion process. However, only sialic acid-independent strains can do so without the presence of glycophorin sialic acid. Our results close a longstanding and important gap in the understanding of the mechanism of erythrocyte invasion by P. falciparum that will eventually make possible the development of an effective blood stage vaccine.
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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.