ArticleParasite immunology2012
CD36 modulates proinflammatory cytokine responses to Plasmodium falciparum glycosylphosphatidylinositols and merozoites by dendritic cells.
Article in Parasite immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Integrating bioinformatics and machine learning to identify glomerular injury genes and predict drug targets in diabetic nephropathy.Scientific reports · 2025Article
- Monocytes, particularly nonclassical ones, lose their opsonic and nonopsonic phagocytosis capacity during pediatric cerebral malaria.Frontiers in immunology · 2024Article
- Microvesicles from malaria-infected red blood cells activate natural killer cells via MDA5 pathway.PLoS pathogens · 2018Article
- The Glycosylphosphatidylinositol Transamidase Complex Subunit PbGPI16 of Plasmodium berghei Is Important for Inducing Experimental Cerebral Malaria.Infection and immunity · 2018Article
- Metabolomic insights of macrophage responses to graphene nanoplatelets: Role of scavenger receptor CD36.PloS one · 2018Article
- CD36 in chronic kidney disease: novel insights and therapeutic opportunities.Nature reviews. Nephrology · 2017Review
- Dendritic cells and parasites: from recognition and activation to immune response instruction.Seminars in immunopathology · 2017Review
- Dendritic Cells and Their Multiple Roles during Malaria Infection.Journal of immunology research · 2016Review
- Host-pathogen interactions in malaria: cross-kingdom signaling and mitochondrial regulation.Current opinion in immunology · 2015Review
- Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Studies have shown that glycosylphosphatidylinositols (GPIs) of Plasmodium falciparum activate macrophages mainly through Toll-like receptor 2 (TLR2)-mediated signalling and to certain extent through TLR4-mediated signalling to induce proinflammatory cytokine production. However, the ability of parasite GPIs to activate dendritic cells (DCs) has not been reported. Here, we show that parasite GPIs efficiently activate DCs through TLR2-mediated signalling mechanism and induce the production of TNF-α and IL-12. We also studied the role of scavenger receptor CD36 in P. falciparum GPI- and merozoite-induced cytokine responses by DCs. The results indicate that CD36 modulates the cytokine-inducing activity of the parasite GPIs by collaborating with TLR2 in DCs. Furthermore, our data reveal that CD36 modulates the activity of P. falciparum merozoites, likely by the contribution of phagocytosis-coupled CD36-mediated signalling to the signalling induced by merozoites. Altogether, these results contribute towards understanding of signalling mechanisms in malaria parasite-induced activation of the innate immune system.
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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.