ArticleJournal of immunology (Baltimore, Md. : 1950)2014
Astrocytic TGF-β signaling limits inflammation and reduces neuronal damage during central nervous system Toxoplasma infection.
Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.
What it found
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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
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Who cites it
92 citing papers in PubMed, 126 citations in OpenAlex.
- Toxoplasma gondii hijacks host S100A6 to enhance cell migration and brain cyst formation.Communications biology · 2026Article
- Targeting Reactive Astrocytes with Flavonoids to Alleviate Neuroinflammation and Promote Synaptic Function.Molecular neurobiology · 2026Review
- Cognitive impairment and prefrontal TGF-β1 elevation in a rat model of fatigue.Frontiers in psychiatry · 2026Article
- Latent Cerebral Toxoplasma Gondii Infection Induces the Kynurenine Pathway and Production of Neurotoxic Metabolites.International journal of tryptophan research : IJTR · 2026Article
- CLEC12A signaling represses protective immune responses and contributes to hippocampal pathology in neurotropic picornavirus infection.Scientific reports · 2025Article
- The Role of Tenascin-C in Neuroinflammation and Neuroplasticity.International journal of molecular sciences · 2025Review
- GSDMD-Deficient G-MDSCs Exert Profoundly Suppressive Activity to Relieve MPTP-Induced Parkinson's Disease.CNS neuroscience & therapeutics · 2025Article
- Multi-Layered Analysis of TGF-β Signaling and Regulation via DNA Methylation and microRNAs in Astrocytic Tumors.International journal of molecular sciences · 2025Article
- Article
- Peripheral Blood-Derived Mesenchymal Stem Cells Promote A2 Phenotype Polarization in Astrocytes via TGF-β-Mediated PI3K/Akt Pathway Activation.European journal of medical research · 2025Article
- Multi-omics profiling of TGF-β isoforms and regulatory miRNAs in astrocytic tumors reveals TGF-β-3 as a prognostic biomarker.Frontiers in oncology · 2025Article
- Tryptophan Metabolism in Alzheimer's Disease with the Involvement of Microglia and Astrocyte Crosstalk and Gut-Brain Axis.Aging and disease · 2024Review
- Evidence for TGF-β1/Nrf2 Signaling Crosstalk in a Cuprizone Model of Multiple Sclerosis.Antioxidants (Basel, Switzerland) · 2024Article
- The Role of Neuromodulation and Potential Mechanism in Regulating Heterotopic Ossification.Neurochemical research · 2024Review
- Adult microglial TGFβ1 is required for microglia homeostasis via an autocrine mechanism to maintain cognitive function in mice.Nature communications · 2024Article
- Review
- Biomaterial strategies for regulating the neuroinflammatory response.Materials advances · 2024Review
- TGF-β signaling in health, disease, and therapeutics.Signal transduction and targeted therapy · 2024Review
- TPN10475 Constrains Effector T Lymphocytes Activation and Attenuates Experimental Autoimmune Encephalomyelitis Pathogenesis by Facilitating TGF-β Signal Transduction.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024Article
- Insights into the glioblastoma tumor microenvironment: current and emerging therapeutic approaches.Frontiers in pharmacology · 2024Review
32 more citing papers are in PubMed but not listed here.
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 4 institutions in 1 country.
Funding
Abstract
The balance between controlling infection and limiting inflammation is particularly precarious in the brain because of its unique vulnerability to the toxic effects of inflammation. Astrocytes have been implicated as key regulators of neuroinflammation in CNS infections, including infection with Toxoplasma gondii, a protozoan parasite that naturally establishes a chronic CNS infection in mice and humans. In CNS toxoplasmosis, astrocytes are critical to controlling parasite growth. They secrete proinflammatory cytokines and physically encircle parasites. However, the molecular mechanisms used by astrocytes to limit neuroinflammation during toxoplasmic encephalitis have not yet been identified. TGF-β signaling in astrocytes is of particular interest because TGF-β is universally upregulated during CNS infection and serves master regulatory and primarily anti-inflammatory functions. We report in this study that TGF-β signaling is activated in astrocytes during toxoplasmic encephalitis and that inhibition of astrocytic TGF-β signaling increases immune cell infiltration, uncouples proinflammatory cytokine and chemokine production from CNS parasite burden, and increases neuronal injury. Remarkably, we show that the effects of inhibiting astrocytic TGF-β signaling are independent of parasite burden and the ability of GFAP(+) astrocytes to physically encircle parasites.
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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.