ArticleMolecular psychiatry2020
Maternal Type-I interferon signaling adversely affects the microglia and the behavior of the offspring accompanied by increased sensitivity to stress.
Article in Molecular psychiatry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
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Who cites it
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.
- The cytokines interleukin-6 and interferon-α induce distinct microglia phenotypes.Journal of neuroinflammation · 2022Pooled it
- Maternal gut microbiota mediates prenatal stress-induced fetal blood‒brain barrier dysfunction.Gut microbes · 2026Article
- Prenatal stress reprograms placental signaling and opposes maternal immune activation effects in the fetal brain.Molecular psychiatry · 2026Article
- Article
- Plasticity of the infant immune system during the perinatal period.Nature reviews. Immunology · 2026Review
- Neurodevelopmental comorbidities in juvenile systemic autoimmune and autoinflammatory diseases.Nature reviews. Rheumatology · 2026Review
- LRRK2 kinase activity restricts NRF2-dependent mitochondrial protection in microglia.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Prenatal Interferon-Alpha Exposure Induces Autism-Like Neurobehavioral and Neurochemical Alterations in Male Offspring.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026Article
- Gestational benzene exposure programs sex-specific neuroimmune responses to postnatal viral infection.Frontiers in immunology · 2026Article
- SARS-CoV-2 vaccination during pregnancy enhances offspring hippocampal neurogenesis and working memory via IFN-γ-responsive microglia.Communications biology · 2025Article
- Microglia determine an immune-challenged environment and facilitate ibuprofen action in human retinal organoids.Journal of neuroinflammation · 2025Article
- Cocaine perturbs neurodevelopment and increases neuroinflammation in a prenatal cerebral organoid model.Translational psychiatry · 2025Article
- IFN-γ signaling links ventriculomegaly to choroid plexus and ependyma dysfunction following maternal immune activation.Journal of neuroinflammation · 2025Article
- Prolonged STAT1 signaling in neurons causes hyperactive behavior.Brain, behavior, and immunity · 2025Article
- The roles of immune factors in neurodevelopment.Frontiers in cellular neuroscience · 2025Review
- Influenza A virus during pregnancy disrupts maternal intestinal immunity and fetal cortical development in a dose- and time-dependent manner.Molecular psychiatry · 2025Article
- The Generation of Genetically Engineered Human Induced Pluripotent Stem Cells Overexpressing IFN-β for Future Experimental and Clinically Oriented Studies.International journal of molecular sciences · 2024Article
- Developmental functions of microglia: Impact of psychosocial and physiological early life stress.Neuropharmacology · 2024Review
- IRF3 regulates neuroinflammatory responses and the expression of genes associated with Alzheimer's disease.Journal of neuroinflammation · 2024Article
- Viral-mediated inflammation by Poly I:C induces the chemokine CCL5 in NK cells and its receptors CCR1 and CCR5 in microglia in the neonatal rat cerebellum.NeuroImmune pharmacology and therapeutics · 2024Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Viral infection during pregnancy is often associated with neuropsychiatric conditions. In mice, exposure of pregnant dams to the viral mimetic poly(I:C), serves as a model that simulates such pathology in the offspring, through a process known as Maternal Immune Activation (MIA). To investigate the mechanism of such effect, we hypothesized that maternal upregulation of Type-I interferon (IFN-I), as part of the dam's antiviral response, might contribute to the damage imposed on the offspring. Using mRNA sequencing and flow cytometry analyses we found that poly(I:C) treatment during pregnancy caused reduced expression of genes related to proliferation and cell cycle in the offspring's microglia relative to controls. This was found to be associated with an IFN-I signature in the embryonic yolk sac, the origin of microglia in development. Neutralizing IFN-I signaling in dams attenuated the effect of MIA on the newborn's microglia, while systemic maternal administration of IFNβ was sufficient to mimic the effect of poly(I:C), and led to increased vulnerability of offspring's microglia to subsequent stress. Furthermore, maternal elevation of IFNβ resulted in behavioral manifestations reminiscent of neuropsychiatric disorders. In addition, by adopting a "two-hit" experimental paradigm, we show a higher sensitivity of the offspring to postnatal stress subsequent to the maternal IFNβ elevation, demonstrated by behavioral irregularities. Our results suggest that maternal upregulation of IFN-I, in response to MIA, interferes with the offspring's programmed microglial developmental cascade, increases their susceptibility to postnatal stress, and leads to behavioral abnormalities.
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