Neuroimmune changes in a mouse model of the maternal infection risk factor for schizophrenia and autism

Objective: Infection in pregnant women is associated with increased risk for autism and schizophrenia in the offspring. In a mouse model of this risk factor, activation of the maternal immune system by injection of the viral mimic poly(I:C) sets in motion a cascade of molecular events that ultimately results in autism- and schizophrenia-related behaviors in offspring. The finding that interleukin-6 (IL-6) is a crucial mediator of these effects led us to examine themechanism by which this cytokine influences fetal development in vivo. Here we examine the placenta and fetal brain as sites of early IL-6 action. We further assess whether MIA offspring display altered postnatal immune profiles and function as a potential later-life consequence of maternal immune activation (MIA).