Viral infection during pregnancy has been suggested to increase the probability of autism spectrum disorder (ASD) in offspring via the phenomenon of maternal immune activation (MIA). This has been modeled in rodents. Maternal T helper 17 cells and the effector cytokine, interleukin 17A (IL-17A), play a central role in MIA-induced behavioral abnormalities and cortical dysgenesis, termed cortical patch. However, it is unclear how IL-17A acts on fetal brain cells to cause ASD pathologies. To assess the effect of IL-17A on cortical development, we directly administered IL-17A into the lateral ventricles of the fetal mouse brain. We analyzed injected brains focusing on microglia, which express IL-17A receptors. We found that IL-17A activated microglia and altered their localization in the cerebral cortex. Our data indicate that IL-17A activates cortical microglia, which leads to a cascade of ASD-related brain pathologies, including excessive phagocytosis of neural progenitor cells in the ventricular zone.

中文翻译：

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脑室内注射IL-17A可激活小胶质细胞并改变其在小鼠胚胎大脑皮层中的定位。

怀孕期间的病毒感染已被建议通过母体免疫激活（MIA）现象增加后代自闭症谱系障碍（ASD）的可能性。这是在啮齿动物中建模的。母体T辅助细胞17和效应细胞因子白介素17A（IL-17A）在MIA诱导的行为异常和皮层发育不全（称为皮层斑）中起着核心作用。然而，尚不清楚IL-17A如何作用于胎儿脑细胞以引起ASD病理。为了评估IL-17A对皮质发育的影响，我们将IL-17A直接施用于胎儿小鼠大脑的侧脑室。我们分析了聚焦于表达IL-17A受体的小胶质细胞的注射大脑。我们发现IL-17A激活了小胶质细胞并改变了它们在大脑皮层中的定位。