ArticleCellular microbiology2016
The Plasmodium falciparum blood stages acquire factor H family proteins to evade destruction by human complement.
Article in Cellular microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 52 citations in OpenAlex.
- Malaria vaccines: Current developments and immunological insights.New microbes and new infections · 2025Article
- Deposition of complement regulators on the surface of Plasmodium falciparum merozoites depends on the immune status of the host.PLoS pathogens · 2025Article
- Malaria: Factors affecting disease severity, immune evasion mechanisms, and reversal of immune inhibition to enhance vaccine efficacy.PLoS pathogens · 2025Review
- Pathogenetic mechanisms and treatment targets in cerebral malaria.Nature reviews. Neurology · 2023Review
- Plasmodium falciparum Gametes and Sporozoites Hijack Plasmin and Factor H To Evade Host Complement Killing.Microbiology spectrum · 2023Article
- Deceiving and escaping complement - the evasive journey of the malaria parasite.Trends in parasitology · 2022Review
- The Defensive Interactions of Prominent Infectious Protozoan Parasites: The Host's Complement System.Biomolecules · 2022Review
- Host-parasite interactions duringFrontiers in immunology · 2022Review
- Factors influencing phagocytosis of malaria parasites: the story so far.Malaria journal · 2021Review
- Is It Possible to Intervene in the Capacity ofFrontiers in immunology · 2021Review
- Interaction Between the Complement System and Infectious Agents - A Potential Mechanistic Link to Neurodegeneration and Dementia.Frontiers in cellular neuroscience · 2021Review
- Hijacking Factor H for Complement Immune Evasion.Frontiers in immunology · 2021Review
- Beyond Binding: The Outcomes of Antibody-Dependent Complement Activation in Human Malaria.Frontiers in immunology · 2021Review
- Complement in malaria: immune evasion strategies and role in protective immunity.FEBS letters · 2020Review
- A receptor for the complement regulator factor H increases transmission of trypanosomes to tsetse flies.Nature communications · 2020Article
- Article
- Complement in malaria immunity and vaccines.Immunological reviews · 2020Review
- Cerebral Plasmodium falciparum malaria: The role of PfEMP1 in its pathogenesis and immunity, and PfEMP1-based vaccines to prevent it.Immunological reviews · 2020Review
- Comprehensive analysis of Fc-mediated IgM binding to the Plasmodium falciparum erythrocyte membrane protein 1 family in three parasite clones.Scientific reports · 2019Article
- Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The acquisition of regulatory proteins is a means of blood-borne pathogens to avoid destruction by the human complement. We recently showed that the gametes of the human malaria parasite Plasmodium falciparum bind factor H (FH) from the blood meal of the mosquito vector to assure successful sexual reproduction, which takes places in the mosquito midgut. While these findings provided a first glimpse of a complex mechanism used by Plasmodium to control the host immune attack, it is hitherto not known, how the pathogenic blood stages of the malaria parasite evade destruction by the human complement. We now show that the human complement system represents a severe threat for the replicating blood stages, particularly for the reinvading merozoites, with complement factor C3b accumulating on the surfaces of the intraerythrocytic schizonts as well as of free merozoites. C3b accumulation initiates terminal complement complex formation, in consequence resulting in blood stage lysis. To inactivate C3b, the parasites bind FH as well as related proteins FHL-1 and CFHR-1 to their surface, and FH binding is trypsin-resistant. Schizonts acquire FH via two contact sites, which involve CCP modules 5 and 20. Blockage of FH-mediated protection via anti-FH antibodies results in significantly impaired blood stage replication, pointing to the plasmodial complement evasion machinery as a promising malaria vaccine target.
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