My research will elucidate the mechanisms by which maternal inflammation can contribute to the development of autism like symptoms in offspring. During pregnancy, a variety of molecules cross the placenta; although most are life-sustaining, some harmful substances also pass through this barrier. In mice, pregnant females that are infected with viruses can give birth to pups that exhibit anxiety, repetitive behaviors, and avoidance of social engagement—actions that resemble the symptoms of autism spectrum disorders in humans. I previously discovered that a particular type of immune cell produced by the mother, called Th17, is involved in this condition: Eliminating these cells from the mother—or blocking the activity of IL-17, an inflammatory chemical they produce—protects the offspring from developing these types of abnormal behaviors. Now, I will determine how IL-17 can cross the placenta from mother to child and how it alters the development of the fetal brain. These findings could lead to an innovative approach to preventing neurodevelopmental disorders, such as autism or schizophrenia, that may be brought about by infection or inflammation in utero.