ArticlePLoS pathogens2014
The CD14+CD16+ inflammatory monocyte subset displays increased mitochondrial activity and effector function during acute Plasmodium vivax malaria.
Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 86 citations in OpenAlex.
- Mitochondrial activity promotes neutrophil degranulation and endothelial dysfunction in systemic infections.EMBO molecular medicine · 2026Article
- Systems approach identifies monocyte imbalance in symptomatic and asymptomatic P. vivax malaria.Molecular systems biology · 2025Article
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- Emerging Role of Splenic Macrophage in Malaria Pathogenesis and Immunity.Immunity, inflammation and disease · 2025Review
- Plasmodium falciparum infection induces T cell tolerance that is associated with decreased disease severity upon re-infection.The Journal of experimental medicine · 2025Article
- Immune regulation of host energy metabolism and periodicity of malaria parasites.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Review
- Extremely low-frequency electromagnetic fields targeting spleen modifies the populations of immunocytes in the spleen.Bioelectromagnetics · 2025Article
- Itaconate impairs immune control of Plasmodium by enhancing mtDNA-mediated PD-L1 expression in monocyte-derived dendritic cells.Cell metabolism · 2024Article
- Monocytes, particularly nonclassical ones, lose their opsonic and nonopsonic phagocytosis capacity during pediatric cerebral malaria.Frontiers in immunology · 2024Article
- A Non-Coding Fc Gamma Receptor Cis-Regulatory Variant within the 1q23 Gene Cluster Is Associated withInternational journal of molecular sciences · 2023Article
- A systematic analysis of the human immune response to Plasmodium vivax.The Journal of clinical investigation · 2023Article
- Distinct immune responses associated with vaccination status and protection outcomes after malaria challenge.PLoS pathogens · 2023Article
- Adenosine pathway regulates inflammation duringFrontiers in immunology · 2023Article
- Malaria Resilience in South America: Epidemiology, Vector Biology, and Immunology Insights from the Amazonian International Center of Excellence in Malaria Research Network in Peru and Brazil.The American journal of tropical medicine and hygiene · 2022Article
- Review
- Activation of cGAS-STING by Lethal Malaria N67C Dictates Immunity and Mortality through Induction of CD11bAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Article
- Factors influencing phagocytosis of malaria parasites: the story so far.Malaria journal · 2021Review
- IFNs Reset the Differential Capacity of Human Monocyte Subsets to Produce IL-12 in Response to Microbial Stimulation.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Disrupted Iron Metabolism and Mortality during Co-infection with Malaria and an Intestinal Gram-Negative Extracellular Pathogen.Cell reports · 2021Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Infection with Plasmodium vivax results in strong activation of monocytes, which are important components of both the systemic inflammatory response and parasite control. The overall goal of this study was to define the role of monocytes during P. vivax malaria. Here, we demonstrate that P. vivax-infected patients display significant increase in circulating monocytes, which were defined as CD14(+)CD16- (classical), CD14(+)CD16(+) (inflammatory), and CD14loCD16(+) (patrolling) cells. While the classical and inflammatory monocytes were found to be the primary source of pro-inflammatory cytokines, the CD16(+) cells, in particular the CD14(+)CD16(+) monocytes, expressed the highest levels of activation markers, which included chemokine receptors and adhesion molecules. Morphologically, CD14(+) were distinguished from CD14lo monocytes by displaying larger and more active mitochondria. CD14(+)CD16(+) monocytes were more efficient in phagocytizing P. vivax-infected reticulocytes, which induced them to produce high levels of intracellular TNF-α and reactive oxygen species. Importantly, antibodies specific for ICAM-1, PECAM-1 or LFA-1 efficiently blocked the phagocytosis of infected reticulocytes by monocytes. Hence, our results provide key information on the mechanism by which CD14(+)CD16(+) cells control parasite burden, supporting the hypothesis that they play a role in resistance to P. vivax infection.
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