ArticleJournal of neuroinflammation2025
IFN-γ signaling links ventriculomegaly to choroid plexus and ependyma dysfunction following maternal immune activation.
Article in Journal of neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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
6 citing papers in PubMed.
- Gasdermin D-Mediated Release of IL-33 Results in Fetal Brain Developmental Abnormalities During Maternal Colitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Temporally Resolved Single-Cell RNA Sequencing Reveals Pathogenesis and Immune Responses in Intracerebral Bacille Calmette-Guérin (BCG) Infection.Pathogens (Basel, Switzerland) · 2026Article
- Ependymal cell inflammatory activation in response to intracerebral hemorrhage.Journal of neuroinflammation · 2026Article
- Microglial Lyn Kinase-TRPV4 axis mediates social deficits in a maternal immune activation model.Journal of neuroinflammation · 2026Article
- Fingolimod Exerts Therapeutic Effects on Autistic Mice via Improving the Structure and Function of Meningeal Lymphatics.CNS neuroscience & therapeutics · 2025Article
- Maternal Immune Activation and Neurodevelopmental Disorders: Integrating Molecular, Cellular and Systems Mechanisms.Neuropsychiatric disease and treatment · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Maternal immune activation (MIA) is a principal environmental risk factor contributing to autism spectrum disorder (ASD) and can be causally linked to ASD symptoms. In our study, we found that MIA triggered by poly (I: C) injection caused ventriculomegaly in offspring due to the dysfunction of the choroid plexus (Chp) and ependyma. We subsequently identified a sustained enhancement of interferon-γ (IFN-γ) signaling in the brain and serum of MIA offspring. Further study revealed that increased IFN-γ signaling could disrupt the barrier function of Chp epithelial cells by activating macrophages, and suppress the differentiation of primary ependymal cells via the signal transducer and activator of transcription 1/3 signaling. The effects of MIA on the offspring were mitigated by administration of IFNGR-blocking antibody in pregnant dams, while systemic maternal administration of IFN-γ was sufficient to mimic the effect of MIA. Overall, our findings revealed that ventriculomegaly caused by IFN-γ signaling could be a critical factor in compromising fetal brain development in MIA-induced ASD and provide a mechanistic framework for the association between maternal inflammation and abnormal development of ventricles in the offspring.
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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.