Modeling maternal immune activation in 3D ex vivo human fetal brain cerebroids reveals IL-17A-driven disruption of cortical development.
- Open access
IL-17A causes premature cortical folding, increased thickness, and accelerated neurogenesis in human fetal brain models, revealing its disruptive role in corticogenesis.
- Why it matters: Understanding how maternal immune activation affects human brain development is crucial for addressing neurodevelopmental disorders linked to immune dysregulation.
- What they did: Researchers developed 'cerebroids,' 3D ex vivo cultures from human fetal cortex, and exposed them to IL-17A, analyzing effects on development, cellular pathways, and signaling mechanisms.
- The result: IL-17A dysregulates extracellular matrix pathways and activates NF-κB signaling in neural stem cells, leading to developmental abnormalities that can be reversed with pathway inhibitors, illuminating potential therapeutic targets.