One theme that emerges from clinical and experimental studies in autism spectrum disorders (ASD) is inflammation and autoimmunity in individuals with ASD and their families. Dr. Ponzio and his colleagues propose to use well-documented experimental models of ASD to test the hypothesis that stimulation of the maternal immune system during pregnancy alters the normal proportions of newly discovered populations of lymphocytes known as T Helper 17 (TH17) cells and T regulatory (Treg) cells, the balance of which may be responsible for determining whether or not the observed neuroinflammation in ASD occurs. Activation of specific types of lymphocytes during an immune response causes secretion of proteins (known as cytokines) that can induce inflammation. If this occurs during pregnancy, these cytokines may cross the placenta, enter the fetus, and influence neural development and cause immunological outcomes and ASD-like behavior patterns in the offspring. This experiment will examine different mechanisms by which cytokine secretions may mediate neural development, including whether or not they alter the placenta, whether they can enter fetal tissues, and if they promote differentiation of immune cells which alter the neuroinflammatory process.