ArticleMolecular psychiatry2023
Human brain organoid model of maternal immune activation identifies radial glia cells as selectively vulnerable.
Article in Molecular psychiatry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 2 of them syntheses that pooled it.
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Who cites it
36 citing papers in PubMed, 2 syntheses or guidelines pooled it, 45 citations in OpenAlex.
- Mapping the Cerebral Organoid Landscape: A Systematic Review of Preclinical 3D Models in Neuroscience.Advanced healthcare materials · 2026Pooled it
- From placenta to the foetus: a systematic review of in vitro models of stress- and inflammation-induced depression in pregnancy.Molecular psychiatry · 2025Pooled it
- Modeling maternal immune activation in 3D ex vivo human fetal brain cerebroids reveals IL-17A-driven disruption of cortical development.Nature neuroscience · 2026Article
- Article
- Maternal immune activation disrupts epigenomic and functional maturation of cortical excitatory neurons.Molecular psychiatry · 2026Article
- Multiomics analysis identifies VPA-induced changes in neural progenitor cells, ventricular-like regions, and cellular microenvironment in dorsal forebrain organoids.Molecular psychiatry · 2026Article
- Dynamic neuro-immune regulation of psychiatric risk loci in human neurons.Nature communications · 2026Article
- Brain organoids and genome editing: A new era in understanding human brain development and disorders.Neural regeneration research · 2026Article
- Modeling Prenatal Immune Activation in Human Brain Organoids Uncovers IL-6-Dependent Interneuron Dysmaturation.bioRxiv : the preprint server for biology · 2026Article
- Neurodevelopmental comorbidities in juvenile systemic autoimmune and autoinflammatory diseases.Nature reviews. Rheumatology · 2026Review
- Article
- Article
- Stem Cell Therapy and Models for Autism Spectrum Disorder: Insights and Research.Current neuropharmacology · 2026Review
- Guided and unguided neural organoids play complementary roles in studying neurodevelopment and neuroinflammation.Einstein (Sao Paulo, Brazil) · 2026Article
- 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
- Molecular and developmental deficits in Smith-Magenis syndrome human stem cell-derived cortical neural models.American journal of human genetics · 2025Article
- Neurodevelopmental Impact of Maternal Immune Activation and Autoimmune Disorders, Environmental Toxicants and Folate Metabolism on Autism Spectrum Disorder.Current issues in molecular biology · 2025Review
- Effect of valproic acid administration on motor coordination and sensory function inOpen veterinary journal · 2025Article
- Human dorsal forebrain organoids show differentiation-state-specific protein secretion.iScience · 2025Article
- Dysregulation of the mTOR-FMRP pathway and synaptic plasticity in an environmental model of ASD.Molecular psychiatry · 2025Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Maternal immune activation (MIA) during critical windows of gestation is correlated with long-term neurodevelopmental deficits in the offspring, including increased risk for autism spectrum disorder (ASD) in humans. Interleukin 6 (IL-6) derived from the gestational parent is one of the major molecular mediators by which MIA alters the developing brain. In this study, we establish a human three-dimensional (3D) in vitro model of MIA by treating induced pluripotent stem cell-derived dorsal forebrain organoids with a constitutively active form of IL-6, Hyper-IL-6. We validate our model by showing that dorsal forebrain organoids express the molecular machinery necessary for responding to Hyper-IL-6 and activate STAT signaling upon Hyper-IL-6 treatment. RNA sequencing analysis reveals the upregulation of major histocompatibility complex class I (MHCI) genes in response to Hyper-IL-6 exposure, which have been implicated with ASD. We find a small increase in the proportion of radial glia cells after Hyper-IL-6 treatment through immunohistochemistry and single-cell RNA-sequencing. We further show that radial glia cells are the cell type with the highest number of differentially expressed genes, and Hyper-IL-6 treatment leads to the downregulation of genes related to protein translation in line with a mouse model of MIA. Additionally, we identify differentially expressed genes not found in mouse models of MIA, which might drive species-specific responses to MIA. Finally, we show abnormal cortical layering as a long-term consequence of Hyper-IL-6 treatment. In summary, we establish a human 3D model of MIA, which can be used to study the cellular and molecular mechanisms underlying the increased risk for developing disorders such as ASD.
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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 OpenQuestion graph.