Microglia, the resident phagocytes of the brain, play a critical role in the fetal brain's response to maternal inflammation. This study shows that microglia are enriched for receptors that respond to pathogens and cytokines involved in maternal immune activation (MIA), which can lead to adverse neuropsychiatric outcomes in offspring. Using a rodent MIA model, the researchers found that MIA induces long-lasting transcriptional changes in fetal microglia that persist into postnatal life. These changes are essential for the transcriptional response of other cortical cell types to MIA, indicating that microglia are necessary for fetal brain development in response to maternal inflammation. The study also identified distinct microglial substates during embryonic development, with some substates expressing receptors for TORCH pathogens and cytokines, suggesting they are poised to respond to inflammatory and infectious insults. The findings highlight the importance of microglia as a potential therapeutic target for preventing and treating adverse neuropsychiatric outcomes in fetuses exposed to maternal infections or inflammatory insults. The study provides a comprehensive map of microglial substates throughout corticogenesis, with high temporal and cell type resolution, and will serve as a resource for future studies of microglial function in both normal development and in disease states.Microglia, the resident phagocytes of the brain, play a critical role in the fetal brain's response to maternal inflammation. This study shows that microglia are enriched for receptors that respond to pathogens and cytokines involved in maternal immune activation (MIA), which can lead to adverse neuropsychiatric outcomes in offspring. Using a rodent MIA model, the researchers found that MIA induces long-lasting transcriptional changes in fetal microglia that persist into postnatal life. These changes are essential for the transcriptional response of other cortical cell types to MIA, indicating that microglia are necessary for fetal brain development in response to maternal inflammation. The study also identified distinct microglial substates during embryonic development, with some substates expressing receptors for TORCH pathogens and cytokines, suggesting they are poised to respond to inflammatory and infectious insults. The findings highlight the importance of microglia as a potential therapeutic target for preventing and treating adverse neuropsychiatric outcomes in fetuses exposed to maternal infections or inflammatory insults. The study provides a comprehensive map of microglial substates throughout corticogenesis, with high temporal and cell type resolution, and will serve as a resource for future studies of microglial function in both normal development and in disease states.