ArticleActa neuropathologica communications2023
Selective neuroimmune modulation by type I interferon drives neuropathology and neurologic dysfunction following traumatic brain injury.
Article in Acta neuropathologica communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 15 citations in OpenAlex.
- Repeated mild spinal cord contusions exacerbate tauopathy development in PS19 mice.Acta neuropathologica communications · 2026Article
- Type I interferon signaling in microglia drives synaptic engulfment and neuronal loss following traumatic brain injury.Research square · 2026Article
- HAPI Cells are SIM-A9-related Mouse Microglial Cells Useful forbioRxiv : the preprint server for biology · 2026Article
- A sex-biased response of the adult brain to Zika virus infection: from down-regulation of neuronal IRF3 to enhanced pathology in adult female mice.Cell communication and signaling : CCS · 2026Article
- Natural killer cells aggravate neuroinflammation through microglial type I interferon pathway activation after traumatic brain injury.Journal of neuroinflammation · 2026Article
- IL-25-ILC2-IL-13 axis improves traumatic brain injury by mediating CXCL-10-dependent regulation of blood brain barrier integrity.Journal of neuroinflammation · 2026Article
- CSF1R and IL1R1 inhibitors synergistically attenuate the early pathogenesis of traumatic brain injury in mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- ADNP is essential for sex-dependent hippocampal neurogenesis, through male unfolded protein response and female mitochondrial gene regulation.Molecular psychiatry · 2025Article
- Diffuse traumatic brain injury induced stimulator of interferons (STING) signaling in microglia drives cortical neuroinflammation, neuronal dysfunction, and impaired cognition.Journal of neuroinflammation · 2025Article
- Diffuse Traumatic Brain Injury Induced Stimulator of Interferons (STING) Signaling in Microglia Drives Cortical Neuroinflammation, Neuronal Dysfunction, and Impaired Cognition.Research square · 2025Article
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- Extracellular cold-inducible RNA-binding protein mediated neuroinflammation and neuronal apoptosis after traumatic brain injury.Burns & trauma · 2024Article
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11 authors at 1 institution in 1 country.
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Abstract
Accumulating evidence suggests that type I interferon (IFN-I) signaling is a key contributor to immune cell-mediated neuropathology in neurodegenerative diseases. Recently, we demonstrated a robust upregulation of type I interferon-stimulated genes in microglia and astrocytes following experimental traumatic brain injury (TBI). The specific molecular and cellular mechanisms by which IFN-I signaling impacts the neuroimmune response and neuropathology following TBI remains unknown. Using the lateral fluid percussion injury model (FPI) in adult male mice, we demonstrated that IFN α/β receptor (IFNAR) deficiency resulted in selective and sustained blockade of type I interferon-stimulated genes following TBI as well as decreased microgliosis and monocyte infiltration. Molecular alteration of reactive microglia also occurred with diminished expression of genes needed for MHC class I antigen processing and presentation following TBI. This was associated with decreased accumulation of cytotoxic T cells in the brain. The IFNAR-dependent modulation of the neuroimmune response was accompanied by protection from secondary neuronal death, white matter disruption, and neurobehavioral dysfunction. These data support further efforts to leverage the IFN-I pathway for novel, targeted therapy of TBI.
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