ArticleNature communications2022
Selective expression of variant surface antigens enables Plasmodium falciparum to evade immune clearance in vivo.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- Rare variable M. tuberculosis antigens induce predominant Th17 responses in human infection.JCI insight · 2026Article
- Inhibitory NK receptor expression associates with altered antimalarial function of γδ T cells.PLoS pathogens · 2026Article
- Hyper-diverse antigenic variation and resilience to transmission-reducing intervention in falciparum malaria.Nature communications · 2024Article
- Hyper-diverse antigenic variation and resilience to transmission-reducing intervention in falciparum malaria.medRxiv : the preprint server for health sciences · 2024Article
- Variable Surface Antigens ofProtein and peptide letters · 2024Review
- Escaping the enemy's bullets: an update on how malaria parasites evade host immune response.Parasitology research · 2023Review
- Predicting Optimal Antimalarial Drug Combinations from a Standardized Plasmodium falciparum Humanized Mouse Model.Antimicrobial agents and chemotherapy · 2023Article
- Host-parasite interactions duringFrontiers in immunology · 2022Review
- Establishment of Humanized Mice for the Study of HBV.Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Plasmodium falciparum has developed extensive mechanisms to evade host immune clearance. Currently, most of our understanding is based on in vitro studies of individual parasite variant surface antigens and how this relates to the processes in vivo is not well-understood. Here, we have used a humanized mouse model to identify parasite factors important for in vivo growth. We show that upregulation of the specific PfEMP1, VAR2CSA, provides the parasite with protection from macrophage phagocytosis and clearance in the humanized mice. Furthermore, parasites adapted to thrive in the humanized mice show reduced NK cell-mediated killing through interaction with the immune inhibitory receptor, LILRB1. Taken together, these findings reveal new insights into the molecular and cellular mechanisms that the parasite utilizes to coordinate immune escape in vivo. Identification and targeting of these specific parasite variant surface antigens crucial for immune evasion provides a unique approach for therapy.
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Registered trials
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