ArticlePloS one2012
IFN-γ signaling to astrocytes protects from autoimmune mediated neurological disability.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 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
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.
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Who cites it
59 citing papers in PubMed, 89 citations in OpenAlex.
- Astrocytes in Multiple Sclerosis: Getting to the Core.International journal of molecular sciences · 2026Review
- Glial cells in chronic inflammation: diversity, dysfunction and therapeutic targeting.Nature reviews. Immunology · 2026Review
- The effect of astrocyte depletion and repopulation approaches in pathological condition of CNS.Acta neurologica Belgica · 2026Review
- Disrupting CSPG-Driven Microglia-Astrocyte Crosstalk Enables Scar-Free Repair in Spinal Cord Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- BATF2 is a regulator of interferon-γ signaling in astrocytes during neuroinflammation.Cell reports · 2025Article
- Astrocytes in aging.Neuron · 2025Review
- Neuroinflammation and neurodegeneration following traumatic brain injuries.Anatomical science international · 2025Review
- Orchestrating Stress Responses in Multiple Sclerosis: A Role for Astrocytic IFNγ Signaling.International journal of molecular sciences · 2024Review
- Article
- Peptide discovery across the spectrum of neuroinflammation; microglia and astrocyte phenotypical targeting, mediation, and mechanistic understanding.Frontiers in molecular neuroscience · 2024Review
- Astrocyte interferon-gamma signaling dampens inflammation during chronic central nervous system autoimmunity via PD-L1.Journal of neuroinflammation · 2023Article
- Prolonged STAT1 activation in neurons drives a pathological transcriptional response.Journal of neuroimmunology · 2023Article
- Intracellular DAMPs in Neurodegeneration and Their Role in Clinical Therapeutics.Molecular neurobiology · 2023Review
- Narrative review of roles of astrocytes in subarachnoid hemorrhage.Annals of translational medicine · 2023Review
- Brain endothelial CXCL12 attracts protective natural killer cells during ischemic stroke.Journal of neuroinflammation · 2023Article
- Astrocytes and Microglia in Stress-Induced Neuroinflammation: The African Perspective.Frontiers in immunology · 2022Review
- Astrocytes and Inflammatory T Helper Cells: A Dangerous Liaison in Multiple Sclerosis.Frontiers in immunology · 2022Review
- Functional immune cell-astrocyte interactions.The Journal of experimental medicine · 2021Review
- Interferon-γ Involvement in the Neuroinflammation Associated with Parkinson's Disease and L-DOPA-Induced Dyskinesia.Neurotoxicity research · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Demyelination and axonal degeneration are determinants of progressive neurological disability in patients with multiple sclerosis (MS). Cells resident within the central nervous system (CNS) are active participants in development, progression and subsequent control of autoimmune disease; however, their individual contributions are not well understood. Astrocytes, the most abundant CNS cell type, are highly sensitive to environmental cues and are implicated in both detrimental and protective outcomes during autoimmune demyelination. Experimental autoimmune encephalomyelitis (EAE) was induced in transgenic mice expressing signaling defective dominant-negative interferon gamma (IFN-γ) receptors on astrocytes to determine the influence of inflammation on astrocyte activity. Inhibition of IFN-γ signaling to astrocytes did not influence disease incidence, onset, initial progression of symptoms, blood brain barrier (BBB) integrity or the composition of the acute CNS inflammatory response. Nevertheless, increased demyelination at peak acute disease in the absence of IFN-γ signaling to astrocytes correlated with sustained clinical symptoms. Following peak disease, diminished clinical remission, increased mortality and sustained astrocyte activation within the gray matter demonstrate a critical role of IFN-γ signaling to astrocytes in neuroprotection. Diminished disease remission was associated with escalating demyelination, axonal degeneration and sustained inflammation. The CNS infiltrating leukocyte composition was not altered; however, decreased IL-10 and IL-27 correlated with sustained disease. These data indicate that astrocytes play a critical role in limiting CNS autoimmune disease dependent upon a neuroprotective signaling pathway mediated by engagement of IFN-γ receptors.
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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.