ArticleEMBO molecular medicine2013
Brain microvessel cross-presentation is a hallmark of experimental cerebral malaria.
Article in EMBO molecular medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 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
103 citing papers in PubMed, 146 citations in OpenAlex.
- CD8+ T cells target cerebrovasculature in children with cerebral malaria.The Journal of clinical investigation · 2020Trial
- Exploring the functions of NKG7 in CD4+ and CD8+ T cells during malaria.PLoS pathogens · 2026Article
- Astrocytic but not Microglial Antigen Presentation Shapes Protective Immunity to Toxoplasma gondii in the Brain.Research square · 2026Article
- Cytotoxic T lymphocytes and their dual role in modulating blood-brain barrier integrity in immune-mediated neurological pathologies.Journal of translational medicine · 2025Review
- Article
- Plasmodium falciparum egress disrupts endothelial junctions and activates JAK-STAT signaling in a microvascular 3D blood-brain barrier model.Nature communications · 2025Article
- CXCL10CNS neuroscience & therapeutics · 2025Article
- Nilotinib attenuates vascular pathology in experimental cerebral malaria.Blood advances · 2025Article
- Severe malaria enforces short-lived effector cell differentiation but does not prevent effective secondary responses by memory CD8 T cells.PLoS pathogens · 2025Article
- The spatiotemporal transcriptional profiling of murine brain during cerebral malaria progression and after artemisinin treatment.Nature communications · 2025Article
- CD8Frontiers in cellular and infection microbiology · 2025Article
- Inflammatory risk contributes to post-COVID endothelial dysfunction through anti-ACKR1 autoantibody.Life science alliance · 2024Article
- Time of day and circadian disruption influence host response and parasite growth in a mouse model of cerebral malaria.iScience · 2024Article
- Beyond the microcirculation: sequestration of infected red blood cells and reduced flow in large draining veins in experimental cerebral malaria.Nature communications · 2024Article
- Discrete class I molecules on brain endothelium differentially regulate neuropathology in experimental cerebral malaria.Brain : a journal of neurology · 2024Article
- Unravelling mysteries at the perivascular space: a new rationale for cerebral malaria pathogenesis.Trends in parasitology · 2024Review
- CD8Frontiers in immunology · 2024Review
- Pathogenetic mechanisms and treatment targets in cerebral malaria.Nature reviews. Neurology · 2023Review
- Neuropilin-1 identifies a subset of highly activated CD8+ T cells during parasitic and viral infections.PLoS pathogens · 2023Article
- The deubiquitinating enzyme OTUD7b protects dendritic cells from TNF-induced apoptosis by stabilizing the E3 ligase TRAF2.Cell death & disease · 2023Article
43 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Cerebral malaria is a devastating complication of Plasmodium falciparum infection. Its pathogenesis is complex, involving both parasite- and immune-mediated events. CD8(+) T cells play an effector role in murine experimental cerebral malaria (ECM) induced by Plasmodium berghei ANKA (PbA) infection. We have identified a highly immunogenic CD8 epitope in glideosome-associated protein 50 that is conserved across rodent malaria species. Epitope-specific CD8(+) T cells are induced during PbA infection, migrating to the brain just before neurological signs manifest. They are functional, cytotoxic and can damage the blood-brain barrier in vivo. Such CD8(+) T cells are also found in the brain during infection with parasite strains/species that do not induce neuropathology. We demonstrate here that PbA infection causes brain microvessels to cross-present parasite antigen, while non-ECM-causing parasites do not. Further, treatment with fast-acting anti-malarial drugs before the onset of ECM reduces parasite load and thus antigen presentation in the brain, preventing ECM death. Thus our data suggest that combined therapies targeting both the parasite and host antigen-presenting cells may improve the outcome of CM patients.
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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.