ArticlePLoS pathogens2017
IL-33 receptor ST2 regulates the cognitive impairments associated with experimental cerebral malaria.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 67 citations in OpenAlex.
- IL-33/ST2 Signaling Sustains Hepato-Intestinal Homeostasis by Orchestrating Vascular Surveillance and Immune Regulatory Circuits During Experimental Trypanosoma cruzi Infection.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Targeting IL-33 in Precision Neuroimmunology: Cellular Mechanisms and Therapeutic Strategies for CNS Disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026Review
- IL-33/ST2 Signaling Protects the Heart by Restraining Inflammation and Parasite Burden duringACS infectious diseases · 2026Article
- β-Dystroglycan Downregulation and Astrocytic Alterations: A Possible Role in Blood-Brain Barrier Disruption During Experimental Cerebral Malaria.Molecular neurobiology · 2025Article
- Electroacupuncture Protects Against Post-stroke Cognitive Impairment by Promoting an IL-33/ST2 Axis-Mediated Microglia M2 Polarization.Neurochemical research · 2025Article
- Cellular Components of the Blood-Brain Barrier and Their Involvement in Aging-Associated Cognitive Impairment.Aging and disease · 2024Review
- Unravelling mysteries at the perivascular space: a new rationale for cerebral malaria pathogenesis.Trends in parasitology · 2024Review
- Critical and diverse role of alarmin cytokines in parasitic infections.Frontiers in cellular and infection microbiology · 2024Review
- Pathogenetic mechanisms and treatment targets in cerebral malaria.Nature reviews. Neurology · 2023Review
- Oligodendrocyte-derived IL-33 functions as a microglial survival factor during neuroinvasive flavivirus infection.PLoS pathogens · 2023Article
- Intrahippocampal Inoculation of AβCells · 2023Article
- Interplay Between the Immune and Nervous Cognitive Systems in Homeostasis and in Malaria.International journal of biological sciences · 2023Review
- The IL-33/ST2 Pathway in Cerebral Malaria.International journal of molecular sciences · 2022Review
- Dual roles of interleukin-33 in cognitive function by regulating central nervous system inflammation.Journal of translational medicine · 2022Review
- Impact of Plasmodium vivax malaria on executive and cognitive functions in elderlies in the Brazilian Amazon.Scientific reports · 2022Article
- Interleukin-33 regulates the functional state of microglia.Frontiers in cellular neuroscience · 2022Review
- Malaria Related Neurocognitive Deficits and Behavioral Alterations.Frontiers in cellular and infection microbiology · 2022Review
- Elevated Plasma Soluble ST2 Levels are Associated With Neuronal Injury and Neurocognitive Impairment in Children With Cerebral Malaria.Pathogens & immunity · 2022Article
- Interrelationship and Sequencing of Interleukins4, 13, 31, and 33 - An Integrated Systematic Review: Dermatological and Multidisciplinary Perspectives.Journal of inflammation research · 2022Review
- P2X Receptor-Dependent Modulation of Mast Cell and Glial Cell Activities in Neuroinflammation.Cells · 2021Review
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebral malaria (CM) is associated with a high mortality rate and long-term neurocognitive impairment in survivors. The murine model of experimental cerebral malaria (ECM) induced by Plasmodium berghei ANKA (PbA)-infection reproduces several of these features. We reported recently increased levels of IL-33 protein in brain undergoing ECM and the involvement of IL-33/ST2 pathway in ECM development. Here we show that PbA-infection induced early short term and spatial memory defects, prior to blood brain barrier (BBB) disruption, in wild-type mice, while ST2-deficient mice did not develop cognitive defects. PbA-induced neuroinflammation was reduced in ST2-deficient mice with low Ifng, Tnfa, Il1b, Il6, CXCL9, CXCL10 and Cd8a expression, associated with an absence of neurogenesis defects in hippocampus. PbA-infection triggered a dramatic increase of IL-33 expression by oligodendrocytes, through ST2 pathway. In vitro, IL-33/ST2 pathway induced microglia expression of IL-1β which in turn stimulated IL-33 expression by oligodendrocytes. These results highlight the IL-33/ST2 pathway ability to orchestrate microglia and oligodendrocytes responses at an early stage of PbA-infection, with an amplification loop between IL-1β and IL-33, responsible for an exacerbated neuroinflammation context and associated neurological and cognitive defects.
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Registered trials
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