ArticleInfection and immunity2014
Damage to the blood-brain barrier during experimental cerebral malaria results from synergistic effects of CD8+ T cells with different specificities.
Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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Who cites it
29 citing papers in PubMed, 39 citations in OpenAlex.
- CCL5 and CD11b-fibrin interactions regulate microglia migration and morphology in hyperinflammatory experimental cerebral malaria.Journal of neuroinflammation · 2026Article
- Article
- Discrete class I molecules on brain endothelium differentially regulate neuropathology in experimental cerebral malaria.Brain : a journal of neurology · 2024Article
- Review
- SARS-CoV-2 Infection Remodels the Phenotype and Promotes Angiogenesis of Primary Human Lung Endothelial Cells.Microorganisms · 2021Article
- Attenuated T Cell Responses Are Associated With the Blockade of Cerebral Malaria Development by YOP1-DeficientFrontiers in immunology · 2021Article
- Using two phases of the CD4 T cell response to blood-stage murine malaria to understand regulation of systemic immunity and placental pathology in Plasmodium falciparum infection.Immunological reviews · 2020Review
- EphA2 contributes to disruption of the blood-brain barrier in cerebral malaria.PLoS pathogens · 2020Article
- Lung endothelial cell antigen cross-presentation to CD8Nature communications · 2019Article
- Co-infection with Chikungunya virus alters trafficking of pathogenic CD8EMBO molecular medicine · 2018Article
- Identification of a Novel CD8 T Cell Epitope Derived fromFrontiers in immunology · 2018Article
- AFrontiers in immunology · 2018Article
- HVEM and CD160: Regulators of Immunopathology During Malaria Blood-Stage.Frontiers in immunology · 2018Article
- Brain Endothelium: The "Innate Immunity Response Hypothesis" in Cerebral Malaria Pathogenesis.Frontiers in immunology · 2018Review
- Profiling MHC II immunopeptidome of blood-stage malaria reveals that cDC1 control the functionality of parasite-specific CD4 T cells.EMBO molecular medicine · 2017Article
- Host Resistance to Plasmodium-Induced Acute Immune Pathology Is Regulated by Interleukin-10 Receptor Signaling.Infection and immunity · 2017Article
- Perforin Expression by CD8 T Cells Is Sufficient To Cause Fatal Brain Edema during Experimental Cerebral Malaria.Infection and immunity · 2017Article
- miR-155 Modifies Inflammation, Endothelial Activation and Blood-Brain Barrier Dysfunction in Cerebral Malaria.Molecular medicine (Cambridge, Mass.) · 2017Article
- Cerebrospinal fluid markers to distinguish bacterial meningitis from cerebral malaria in children.Wellcome open research · 2017Article
- The Deubiquitinating Enzyme Cylindromatosis Dampens CD8Frontiers in immunology · 2017Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CD8(+) T cells play a pathogenic role in the development of murine experimental cerebral malaria (ECM) induced by Plasmodium berghei ANKA (PbA) infection in C57BL/6 mice. Only a limited number of CD8(+) epitopes have been described. Here, we report the identification of a new epitope from the bergheilysin protein recognized by PbA-specific CD8(+) T cells. Induction and functionality of these specific CD8(+) T cells were investigated in parallel with previously reported epitopes, using new tools such as tetramers and reporter cell lines that were developed for this study. We demonstrate that CD8(+) T cells of diverse specificities induced during PbA infection share many characteristics. They express cytolytic markers (gamma interferon [IFN-γ], granzyme B) and chemokine receptors (CXCR3, CCR5) and damage the blood-brain barrier in vivo. Our earlier finding that brain microvessels in mice infected with PbA, but not with non-ECM-causing strains, cross-presented a shared epitope was generalizable to these additional epitopes. Suppressing the induction of specific CD8(+) T cells through tolerization with a high-dose peptide injection was unable to confer protection against ECM, suggesting that CD8(+) T cells of other specificities participate in this process. The tools that we developed can be used to further investigate the heterogeneity of CD8(+) T cell responses that are involved in ECM.
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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.