ArticlePLoS pathogens2015
IL-33-mediated protection against experimental cerebral malaria is linked to induction of type 2 innate lymphoid cells, M2 macrophages and regulatory T cells.
Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.
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Who cites it
95 citing papers in PubMed, 146 citations in OpenAlex.
- The Role of the IL-33/ST2 Axis in Nervous System Development and Diseases.Immunology and cell biology · 2026Review
- 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
- Association of interleukin-33 gene polymorphisms with susceptibility to Plasmodium falciparum infection.Malaria journal · 2026Article
- Hdac11 promotes idiopathic pulmonary fibrosis through macrophage M2-type polarization and myofibroblast accumulation by inhibiting Parkin-dependent mitophagy.Nature communications · 2026Article
- IL-33/ST2 Signaling Protects the Heart by Restraining Inflammation and Parasite Burden duringACS infectious diseases · 2026Article
- Malaria pigment hemozoin drives M1 pro-inflammatory macrophage polarization in vitro.Scientific reports · 2025Article
- GSDME-dependent astrocyte pyroptosis promotes the progression of neuroinflammation in experimental cerebral malaria.Apoptosis : an international journal on programmed cell death · 2025Article
- The Multifaceted Role of Regulatory T Cells in Sepsis: Mechanisms, Heterogeneity, and Pathogen-Tailored Therapies.International journal of molecular sciences · 2025Review
- Analysis of immune infiltration in basal cell carcinoma based on transcriptome sequencing and experimental validation of diagnostic biomarkers.Discover oncology · 2025Article
- Microbiome-mediated modulation of immune memory to P. yoelii affects the resistance to secondary cerebral malaria challenge.ImmunoHorizons · 2025Article
- IL-33/ST2 axis in diverse diseases: regulatory mechanisms and therapeutic potential.Frontiers in immunology · 2025Review
- Dynamics of tissue repair regulatory T cells and damage in acute Trypanosoma cruzi infection.PLoS pathogens · 2025Article
- IL-33 deficiency inhibits Toxoplasma gondii infection by promoting NLRP3 inflammasome.Parasitology research · 2024Article
- Administration of rIL-33 Restores Altered mDC/pDC Ratio, MDSC Frequency, and Th-17/Treg Ratio during Experimental Cerebral Malaria.Pathogens (Basel, Switzerland) · 2024Article
- Blockage of mechanosensitive Piezo1 channel alleviates the severity of experimental malaria-associated acute lung injury.Parasites & vectors · 2024Article
- NK cells contribute to the resolution of experimental malaria-associated acute respiratory distress syndrome after antimalarial treatment.Frontiers in immunology · 2024Article
- 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
- Group 2 innate lymphoid cells resolve neuroinflammation following cerebral ischaemia.Stroke and vascular neurology · 2023Article
35 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
Abstract
Cerebral malaria (CM) is a complex parasitic disease caused by Plasmodium sp. Failure to establish an appropriate balance between pro- and anti-inflammatory immune responses is believed to contribute to the development of cerebral pathology. Using the blood-stage PbA (Plasmodium berghei ANKA) model of infection, we show here that administration of the pro-Th2 cytokine, IL-33, prevents the development of experimental cerebral malaria (ECM) in C57BL/6 mice and reduces the production of inflammatory mediators IFN-γ, IL-12 and TNF-α. IL-33 drives the expansion of type-2 innate lymphoid cells (ILC2) that produce Type-2 cytokines (IL-4, IL-5 and IL-13), leading to the polarization of the anti-inflammatory M2 macrophages, which in turn expand Foxp3 regulatory T cells (Tregs). PbA-infected mice adoptively transferred with ILC2 have elevated frequency of M2 and Tregs and are protected from ECM. Importantly, IL-33-treated mice deleted of Tregs (DEREG mice) are no longer able to resist ECM. Our data therefore provide evidence that IL-33 can prevent the development of ECM by orchestrating a protective immune response via ILC2, M2 macrophages and Tregs.
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