ArticlePLoS pathogens2020
Astrocytes promote a protective immune response to brain Toxoplasma gondii infection via IL-33-ST2 signaling.
Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 45 citations in OpenAlex.
- IL-33 as a boundary-tissue state-transfer signal: a Reader-Alarmin-Effector architecture linking CNS and skin.Brain, behavior, & immunity - health · 2026Review
- ZBP1 mediated restriction of Toxoplasma gondii in both the early acute and chronic brain stages of infection.ImmunoHorizons · 2026Article
- Caspase-8 expression in CD8Science advances · 2025Article
- Article
- Article
- IL-33 deficiency inhibits Toxoplasma gondii infection by promoting NLRP3 inflammasome.Parasitology research · 2024Article
- Immunomodulation by the combination of statin and matrix-bound nanovesicle enhances optic nerve regeneration.NPJ Regenerative medicine · 2024Article
- Caspase-1 in Cx3cr1-expressing cells drives an IL-18-dependent T cell response that promotes parasite control during acute Toxoplasma gondii infection.PLoS pathogens · 2024Article
- Protective function and differentiation cues of brain-resident CD8+ T cells during surveillance of latentProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Glia Maturation Factor Beta: A Novel Neuro-Impairment Prediction Factor in Toxoplasmosis.Iranian journal of public health · 2024Article
- Pathological mechanisms of glial cell activation and neurodegenerative and neuropsychiatric disorders caused byFrontiers in microbiology · 2024Review
- Critical and diverse role of alarmin cytokines in parasitic infections.Frontiers in cellular and infection microbiology · 2024Review
- Deficiency in astrocyte CCL2 production reduces neuroimmune control of Toxoplasma gondii infection.PLoS pathogens · 2024Article
- Oligodendrocyte-derived IL-33 functions as a microglial survival factor during neuroinvasive flavivirus infection.PLoS pathogens · 2023Article
- The gut microbiome regulates astrocyte reaction to Aβ amyloidosis through microglial dependent and independent mechanisms.Molecular neurodegeneration · 2023Article
- Regulatory Functions of Hypoxia in Host-Parasite Interactions: A Focus on Enteric, Tissue, and Blood Protozoa.Microorganisms · 2023Review
- IL-18BP mediates the balance between protective and pathological immune responses to Toxoplasma gondii.Cell reports · 2023Article
- Cerebral toxoplasmosis in HIV-infected patients: a review.Pathogens and global health · 2023Review
- Article
- TSLP, IL-33, and IL-25: Not just for allergy and helminth infection.The Journal of allergy and clinical immunology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
It is of great interest to understand how invading pathogens are sensed within the brain, a tissue with unique challenges to mounting an immune response. The eukaryotic parasite Toxoplasma gondii colonizes the brain of its hosts, and initiates robust immune cell recruitment, but little is known about pattern recognition of T. gondii within brain tissue. The host damage signal IL-33 is one protein that has been implicated in control of chronic T. gondii infection, but, like many other pattern recognition pathways, IL-33 can signal peripherally, and the specific impact of IL-33 signaling within the brain is unclear. Here, we show that IL-33 is expressed by oligodendrocytes and astrocytes during T. gondii infection, is released locally into the cerebrospinal fluid of T. gondii-infected animals, and is required for control of infection. IL-33 signaling promotes chemokine expression within brain tissue and is required for the recruitment and/or maintenance of blood-derived anti-parasitic immune cells, including proliferating, IFN-γ-expressing T cells and iNOS-expressing monocytes. Importantly, we find that the beneficial effects of IL-33 during chronic infection are not a result of signaling on infiltrating immune cells, but rather on radio-resistant responders, and specifically, astrocytes. Mice with IL-33 receptor-deficient astrocytes fail to mount an adequate adaptive immune response in the CNS to control parasite burden-demonstrating, genetically, that astrocytes can directly respond to IL-33 in vivo. Together, these results indicate a brain-specific mechanism by which IL-33 is released locally, and sensed locally, to engage the peripheral immune system in controlling a pathogen.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.