Autism spectrum disorder (ASD) is one of the most prevalent and debilitating disorders for patients and their family members. Understanding the neural mechanisms of ASD will greatly facilitate the development of novel ways to prevent and treat ASD. Severe infection in mothers during pregnancy is correlated with increased incident of ASD in offspring. Consistent with human studies, maternal immune activation (MIA) model in rodents also induces autism-like phenotypes in offspring. Recently, our group demonstrated that the interleukin receptor 17a (IL- 17Ra) pathway is necessary for the development of cortical lamination and autism-like behavioral phenotypes in MIA offspring. Here, I propose to investigate the role of IL- 17Ra in the brain development of normal and MIA-affected offspring, as well as the mechanisms behind the abnormal cortical lamination seen in MIA offspring, focusing on neuronal migration. My first two goals for this experiment will be to characterize the adhesive properties of IL-17Ra during brain development, and then to identify binding partners of IL-17Ra during neuronal migration. I hope these results will demonstrate a novel role of the immune system in brain development and aid in the development of mechanism-based interventions for MIA-induced ASD.