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Related Experiment Video

Updated: May 15, 2026

Generating a Reproducible Model of Mid-Gestational Maternal Immune Activation using Poly(I:C) to Study Susceptibility and Resilience in Offspring
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Generating a Reproducible Model of Mid-Gestational Maternal Immune Activation using Poly(I:C) to Study Susceptibility and Resilience in Offspring

Published on: August 17, 2022

Maternal immune activation perturbs the brain epitranscriptome.

Shin Jeon1, Bharti Kukreja2, Juneil Jang1

  • 1Department of Systems Pharmacology and Translational Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA; Institute for Immunology and Immune Health, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.

Brain, Behavior, and Immunity
|May 13, 2026
PubMed
Summary
This summary is machine-generated.

Maternal immune activation disrupts fetal brain development by altering RNA metabolism. Targeting the FTO enzyme can potentially correct these neurodevelopmental deficits in offspring.

Keywords:
EpitranscriptomeMaternal immune activationSpatial transcriptomicsTranslation

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Published on: March 25, 2016

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Last Updated: May 15, 2026

Generating a Reproducible Model of Mid-Gestational Maternal Immune Activation using Poly(I:C) to Study Susceptibility and Resilience in Offspring
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Generating a Reproducible Model of Mid-Gestational Maternal Immune Activation using Poly(I:C) to Study Susceptibility and Resilience in Offspring

Published on: August 17, 2022

Induction of Maternal Immune Activation in Mice at Mid-gestation Stage with Viral Mimic Poly(I:C)
07:13

Induction of Maternal Immune Activation in Mice at Mid-gestation Stage with Viral Mimic Poly(I:C)

Published on: March 25, 2016

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Molecular Biology

Background:

  • Maternal immune activation (MIA) is linked to neurodevelopmental disorders.
  • Altered RNA translation contributes to MIA-associated neurodevelopmental deficits.
  • Precise mechanisms of RNA metabolism disruption in MIA remain unclear.

Purpose of the Study:

  • To characterize the RNA epitranscriptomic machinery in the developing mouse brain.
  • To investigate how MIA impacts the brain epitranscriptome.
  • To identify and target specific regulators for therapeutic intervention.

Main Methods:

  • Spatial transcriptomics to map epitranscriptome regulators.
  • Direct RNA sequencing to analyze MIA-induced epitranscriptome changes.
  • Pharmacological and genetic targeting of FTO in mouse models.

Main Results:

  • Defined cell type- and brain region-specific distribution of epitranscriptome regulators.
  • Identified significant perturbation of the FTO demethylase in MIA.
  • Demonstrated that targeting FTO ameliorates behavioral phenotypes in MIA offspring.

Conclusions:

  • MIA disrupts RNA metabolism and translational regulation in the developing brain.
  • FTO is a key mediator of MIA-induced neurodevelopmental alterations.
  • Targeting FTO offers a potential therapeutic strategy for MIA-associated neurodevelopmental disorders.