ArticleCNS neuroscience & therapeutics2024
Microglial priming by IFN-γ involves STAT1-mediated activation of the NLRP3 inflammasome.
Article in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Article
- Post-translational modifications in Neuroimmune cells during neuroinflammation: integrated regulatory networks and therapeutic opportunities.Biology direct · 2026Review
- Article
- Systems biology-based drug repurposing for neuroinflammation treatment in activated human microglia.Scientific reports · 2026Article
- 1 Hz Low-Frequency Repetitive Transcranial Magnetic Stimulation Ameliorates Epilepsy by Suppressing Interferon-γ Signaling-Dependent Microglial Synaptic Phagocytosis in Mice.CNS neuroscience & therapeutics · 2026Article
- Immunotherapy for depression: targeting cytokine pathways in major depressive disorder.Psychopharmacology · 2026Review
- Immune imbalance between T helper 1, T helper 17 and regulatory T cells fuels amyotrophic lateral sclerosis pathogenesis: disease trajectory, diagnosis and therapeutic implications.Journal of neuroinflammation · 2026Review
- Targeting the CCL7-STAT1 axis attenuates microglial neurotoxicity and photoreceptor degeneration in retinitis pigmentosa.Journal of neuroinflammation · 2026Article
- Dual NLRC4 and non-canonical inflammasome signaling drives human GSDMD-mediated killing ofbioRxiv : the preprint server for biology · 2026Article
- Research advances on NLRP3 inflammasomes in organ transplantation.Frontiers in immunology · 2026Review
- Innate Immune Tolerance Regulates Microglia Response to Aβ Oligomers.Journal of neurochemistry · 2026Article
- SIRT1 deacetylates GAPDH to drive microglial glycolysis and neuroinflammation.Frontiers in immunology · 2026Article
- A diagnostic model of atherosclerosis based on the oxidative stress-glycolysis co-regulatory network.Molecular and cellular biochemistry · 2026Article
- Microglial histone H3K18 crotonylation promotes STAT1 expression and induces cognitive deficit in Alzheimer disease.Frontiers in immunology · 2026Article
- Microglial Polarization and Therapeutic Strategies in Post-stroke Neuroinflammation.Neurology and therapy · 2025Review
- Modeling Pain Without Injury: Inherited Rodent Models as Mechanistic Windows into Chronic Pain.Function (Oxford, England) · 2025Review
- Involvement of Matrix Metalloproteinases (MMP-2 and MMP-9), Inflammasome NLRP3, and Gamma-Aminobutyric Acid (GABA) Pathway in Cellular Mechanisms of Neuroinflammation in PTSD.International journal of molecular sciences · 2025Article
- Escherichia Coli K1-colibactin meningitis induces microglial NLRP3/IL-18 exacerbating H3K4me3-synucleinopathy in human inflammatory gut-brain axis.Communications biology · 2025Article
- Decoding Fibromyalgia: Genetic Insights into Gut and Immune System Interactions.Journal of pain research · 2025Article
- NLRP3 Inflammasome Activation in Liver Disorders: From Molecular Pathways to Therapeutic Strategies.Journal of inflammation research · 2025Review
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9 authors.
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Abstract
backgroundInflammatory and immune responses in the brain that contribute to various neuropsychiatric disorders may begin as microglial "priming". Interferon (IFN)-γ is known to cause microglial priming, but the mechanism is unclear.
methodsWe examined the effects of IFN-γ on gene expression, microglial activation, inflammatory and immune responses and activity of the NLRP3 inflammasome in primary microglia and in the brains of mice.
resultsOur results showed that treating microglial cultures with IFN-γ induced a hedgehog-like morphology and upregulated markers of microglial activation (CD86, CD11b) and pro-inflammatory molecules (IL-1β, IL-6, TNF-α, iNOS), while downregulating markers of microglial homeostasis (CX3CR1, CD200R1), anti-inflammatory molecules (MCR1, Arg-1) and neurotrophic factors (IGF-1, BDNF). IFN-γ also upregulated markers of NLRP3 inflammasome activation (NLRP3, caspase-1, gasdermin D, IL-18). This particular transcriptional profiling makes IFN-γ-primed microglia with exaggerated responses upon lipopolysaccharide (LPS) stimulation. The level of NLRP3, caspase-1, gasdermin D, IL-1β, IL-18, TNF-α and iNOS in microglia cultures treated with both IFN-γ and LPS were highest than with either one alone. Injecting IFN-γ into the lateral ventricle of mice induced similar morphological and functional changes in hippocampal microglia as in primary microglial cultures. The effects of IFN-γ on NLRP3 inflammasome and microglia from cultures or hippocampus were abolished when STAT1 was inhibited using fludarabin. Injecting mice with IFN-γ alone or together with LPS induced anxiety- and depression-like behaviors and impaired hippocampus-dependent spatial memory; these effects were mitigated by fludarabin.
conclusionsIFN-γ primes microglia by activating STAT1, which upregulates genes that activate the NLRP3 inflammasome. Inhibiting the IFN-γ/STAT1 axis may be a way to treat neurodegenerative diseases and psychiatric disorders that involve microglial priming.
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