ArticleMolecular psychiatry2025
Embryo-restricted responses to maternal IL-17A promote neurodevelopmental disorders in mouse offspring.
Article in Molecular psychiatry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Cerebellar microglia-derived IL-17A mitigates autism-related behavioral and synaptic deficits.Molecular psychiatry · 2026Article
- Gestational Hypertension as a Mediator of Prenatal Ozone Exposure and Term Low Birth Weight: Birth Cohort Study.JMIR public health and surveillance · 2026Article
- Maternal Poly (I:C)-Induced Placental Inflammation and Endocrine Dysfunction Are Associated with Disrupted Corticogenesis in Mouse Offspring.Brain sciences · 2026Article
- Neuroinflammatory mechanisms and pharmacological advances in autism spectrum disorder: from inflammatory pathways to targeted interventions.Frontiers in immunology · 2026Review
- Gestational hypothyroxinemia causes an inflammatory environment at maternal-fetal tissues and fetal brain with impaired hippocampal dendritic spine maturation in the offspring.Scientific reports · 2025Article
- Double-hit of MIA and Nod2 deficiency induces sex-specific offspring behavioral abnormalities through placental dysregulation.Translational psychiatry · 2025Article
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Authors and funding
11 authors.
Funding
Abstract
Prenatal imprinting to interleukin 17A (IL-17A) triggers behavioral disorders in offspring. However, reported models of maternal immune activation utilizing immunostimulants, lack specificity to elucidate the anatomical compartments of IL-17A's action and the distinct behavioral disturbances it causes. By combining transgenic IL-17A overexpression with maternal deficiency in its receptor, we established a novel model of prenatal imprinting to maternal IL-17A (acronym: PRIMA-17 model). This model allowed us to study prenatal imprinting established exclusively through embryo-restricted IL-17A responses. We demonstrated a transfer of transgenic IL-17A across the placental barrier, which triggered the development of selected behavioral deficits in mouse offspring. More specifically, embryonic responses to IL-17A resulted in communicative impairment in early-life measured by reduced numbers of nest retrieval calls. In adulthood, IL-17A-imprinted offspring displayed an increase in anxiety-like behavior. We advocate our PRIMA-17 model as a useful tool to study neurological deficits in mice.
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