ArticleJournal of neuroimmunology2023
Prolonged STAT1 activation in neurons drives a pathological transcriptional response.
Article in Journal of neuroimmunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 18 citations in OpenAlex.
- Getting on your last nerve: IFNs and resistance to infection.Journal of immunology (Baltimore, Md. : 1950) · 2026Review
- IFN-γ increases δ-globin gene expression through activation of the JAK/STAT pathway in erythroid cells.Blood · 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
- Dual role of IFNγ in reprogramming the undifferentiated pleomorphic sarcoma cell line JBT19 towards cytotoxic chemotherapy and antitumor immunity.Oncology letters · 2026Article
- Targeting the CCL7-STAT1 axis attenuates microglial neurotoxicity and photoreceptor degeneration in retinitis pigmentosa.Journal of neuroinflammation · 2026Article
- From bugs to behavior: targeting the gut-brain interface for addiction therapeutics.Gut microbes · 2025Review
- Intraventricular Creatine Treatment Attenuates Alzheimer's Disease-Related Neuropathological Changes and Memory Impairment via Inhibiting STAT1 Phosphorylation.ACS chemical neuroscience · 2025Article
- Article
- The intersection of endocrine signaling and neuroimmune communication regulates muscle inflammation-induced nociception in neonatal mice.Brain, behavior, and immunity · 2025Article
- Prolonged STAT1 signaling in neurons causes hyperactive behavior.Brain, behavior, and immunity · 2025Article
- STAT1 and herpesviruses: Making lemonade from lemons.Virology · 2025Review
- The neuropathobiology of multiple sclerosis.Nature reviews. Neuroscience · 2024Review
- Analysis of intestinal epithelial cell responses to Cryptosporidium highlights the temporal effects of IFN-γ on parasite restriction.PLoS pathogens · 2024Article
- The interplay between the microbiota and opioid in the treatment of neuropathic pain.Frontiers in microbiology · 2024Review
- Neuroplasticity of children in autism spectrum disorder.Frontiers in psychiatry · 2024Review
- Lactobacillus from the Altered Schaedler Flora maintain IFNγ homeostasis to promote behavioral stress resilience.Brain, behavior, and immunity · 2024Article
- Analysis of intestinal epithelial cell responses tobioRxiv : the preprint server for biology · 2023Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Neurons require physiological IFN-γ signaling to maintain central nervous system (CNS) homeostasis, however, pathological IFN-γ signaling can cause CNS pathologies. The downstream signaling mechanisms that cause these drastically different outcomes in neurons has not been well studied. We hypothesized that different levels of IFN-γ signaling in neurons results in differential activation of its downstream transcription factor, signal transducer and activator of transduction 1 (STAT1), causing varying outcomes. Using primary cortical neurons, we showed that physiological IFN-γ elicited brief and transient STAT1 activation, whereas pathological IFN-γ induced prolonged STAT1 activation, which primed the pathway to be more responsive to a subsequent IFN-γ challenge. This is an IFN-γ specific response, as other IFNs and cytokines did not elicit such STAT1 activation nor priming in neurons. Additionally, we did not see the same effect in microglia or astrocytes, suggesting this non-canonical IFN-γ/STAT1 signaling is unique to neurons. Prolonged STAT1 activation was facilitated by continuous janus kinase (JAK) activity, even in the absence of IFN-γ. Finally, although IFN-γ initially induced a canonical IFN-γ transcriptional response in neurons, pathological levels of IFN-γ caused long-term changes in synaptic pathway transcripts. Overall, these findings suggest that IFN-γ signaling occurs via non-canonical mechanisms in neurons, and differential STAT1 activation may explain how neurons have both homeostatic and pathological responses to IFN-γ signaling.
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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 Socratic graph.