Neurodevelopment is a highly orchestrated and precisely timed process that displays vulnerability towards environmental insults. Maternal immune activation (MIA) during gestation can disturb this delicate balance and increase the offsprings risk for neurodevelopmental disorders like schizophrenia and autism later in life.This study investigates the differential impact of MIA on neuronal progenitor cells at E10.5 (polyI:C administration at E9.5) by using single-cell RNA sequencing. Additionally, we examined the role of microglia in mediating the effects of MIA at different developmental stages.Tbr1+ immature principal neurons were particularly affected by MIA, exhibiting reduced abundance. GSEA showed downregulation of GO terms associated with crucial neurodevelopmental processes across cell types in the MIA-treated samples. In contrast, upregulated GO terms were linked to cellular stress response, including unfolded protein response and ER stress. Microglia appeared to play a minor role at mediating the effect of MIA at this early developmental timepoint of E10.5. Also, IL-17a blocking failed to rescue the proliferation defect observed in the medial ganglionic eminence (MGE) at E10.5. Interestingly, at E13.5 (polyI:C administration at E12.5) microglia depletion and MIA resulted in the same proliferation defect in the GEs, suggesting shared pathways.We showed that MIA changes the fate of immature principal neurons and impacts neuronal progenitor cells of the inhibitory lineage even at early developmental stages, potentially independent of microglial. At a later stage, it appears that microglial (dys-)function is important in mediating the effect of MIA.