ArticleInfection and immunity2017
Gamma Interferon Mediates Experimental Cerebral Malaria by Signaling within Both the Hematopoietic and Nonhematopoietic Compartments.
Article in Infection and immunity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- IFN-γ drives inflammatory bowel disease pathogenesis through VE-cadherin-directed vascular barrier disruption.The Journal of clinical investigation · 2019Trial
- Inflame and restrain - the paradoxical roles of IL-12 and IL-23 in immunity.Nature reviews. Immunology · 2026Review
- Article
- The spatiotemporal transcriptional profiling of murine brain during cerebral malaria progression and after artemisinin treatment.Nature communications · 2025Article
- Pathogenetic mechanisms and treatment targets in cerebral malaria.Nature reviews. Neurology · 2023Review
- Article
- Interplay Between the Immune and Nervous Cognitive Systems in Homeostasis and in Malaria.International journal of biological sciences · 2023Review
- Model of severe malaria in young mice suggests unique response of CD4 T cells.Parasite immunology · 2022Article
- Review
- Cerebral Malaria: Current Clinical and Immunological Aspects.Frontiers in immunology · 2022Review
- Mannose inhibitsFrontiers in immunology · 2022Article
- Suppression of Plasmodium MIF-CD74 signaling protects against severe malaria.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Memory CD8Immunology · 2021Article
- Insilico Functional Analysis of Genome-Wide Dataset From 17,000 Individuals Identifies Candidate Malaria Resistance Genes Enriched in Malaria Pathogenic Pathways.Frontiers in genetics · 2021Article
- Eosinophils Suppress the Migration of T Cells Into the Brain ofFrontiers in immunology · 2021Article
- Attenuated T Cell Responses Are Associated With the Blockade of Cerebral Malaria Development by YOP1-DeficientFrontiers in immunology · 2021Article
- Integrative analysis of microRNA and mRNA expression profiles of monocyte-derived dendritic cells differentiation during experimental cerebral malaria.Journal of leukocyte biology · 2020Article
- Article
- γδ-T cells promote IFN-γ-dependentProceedings of the National Academy of Sciences of the United States of America · 2019Article
- TRPV1 Contributes to Cerebral Malaria Severity and Mortality by Regulating Brain Inflammation.Oxidative medicine and cellular longevity · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Experimental cerebral malaria (ECM) is a gamma interferon (IFN-γ)-dependent syndrome. However, whether IFN-γ promotes ECM through direct and synergistic targeting of multiple cell populations or by acting primarily on a specific responsive cell type is currently unknown. Here, using a panel of cell- and compartment-specific IFN-γ receptor 2 (IFN-γR2)-deficient mice, we show that IFN-γ causes ECM by signaling within both the hematopoietic and nonhematopoietic compartments. Mechanistically, hematopoietic and nonhematopoietic compartment-specific IFN-γR signaling exerts additive effects in orchestrating intracerebral inflammation, leading to the development of ECM. Surprisingly, mice with specific deletion of IFN-γR2 expression on myeloid cells, T cells, or neurons were completely susceptible to terminal ECM. Utilizing a reductionist
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.