A maternal interleukin-17a (IL-17a) pathway promotes autism-like phenotypes in offspring. This study shows that maternal IL-17a, produced by T helper 17 (T_H17) cells, is critical for the development of autism-like behaviors and cortical abnormalities in offspring of pregnant mice exposed to maternal immune activation (MIA). MIA, which mimics viral infection, leads to increased levels of IL-17a in the mother, which then affects fetal brain development. The study demonstrates that maternal T_H17 cells and IL-17a are essential for the induction of ASD-like phenotypes in offspring. Blocking IL-17a signaling in pregnant mothers reduces the likelihood of offspring developing these phenotypes. The research also shows that maternal IL-17a contributes to abnormal cortical development in the fetus, which is rescued by inhibiting the maternal IL-17a pathway. Additionally, the study finds that IL-17a acts directly on the fetal brain to induce abnormal cortical development and ASD-like behaviors. Therapeutic targeting of the IL-17a pathway in pregnant mothers may help prevent the development of ASD-like phenotypes in offspring. The findings suggest that the maternal immune system, particularly the IL-17a pathway, plays a significant role in the development of autism-like behaviors and cortical abnormalities in offspring. The study highlights the importance of understanding the role of the maternal immune system in neurodevelopmental disorders.A maternal interleukin-17a (IL-17a) pathway promotes autism-like phenotypes in offspring. This study shows that maternal IL-17a, produced by T helper 17 (T_H17) cells, is critical for the development of autism-like behaviors and cortical abnormalities in offspring of pregnant mice exposed to maternal immune activation (MIA). MIA, which mimics viral infection, leads to increased levels of IL-17a in the mother, which then affects fetal brain development. The study demonstrates that maternal T_H17 cells and IL-17a are essential for the induction of ASD-like phenotypes in offspring. Blocking IL-17a signaling in pregnant mothers reduces the likelihood of offspring developing these phenotypes. The research also shows that maternal IL-17a contributes to abnormal cortical development in the fetus, which is rescued by inhibiting the maternal IL-17a pathway. Additionally, the study finds that IL-17a acts directly on the fetal brain to induce abnormal cortical development and ASD-like behaviors. Therapeutic targeting of the IL-17a pathway in pregnant mothers may help prevent the development of ASD-like phenotypes in offspring. The findings suggest that the maternal immune system, particularly the IL-17a pathway, plays a significant role in the development of autism-like behaviors and cortical abnormalities in offspring. The study highlights the importance of understanding the role of the maternal immune system in neurodevelopmental disorders.