Inflammation during pregnancy has been suggested as a possible contributing factor in the development of autism spectrum disorders in children. A replica of this phenomenon, called the maternal immune activation (MIA) model, is used to study inflammation-induced behavioral changes in rodents. Identification of key immune components in the MIA model may lead to a better understanding of underlying causes of autism.

Dan Littman and his colleagues at New York University School of Medicine study the molecular mechanisms of inflammation that are mediated by immune cells. They have identified a key factor called ROR gamma-t that is required in the development of pro-inflammatory T cells, which play crucial roles in various autoimmune diseases. These cells, called Th17 cells, may also have important functions in the progression of MIA in pregnant rodents.

Preliminary results support the hypothesis that Th17 cells in the mother mediate behavioral changes in the offspring, according to the MIA model. Littman and his team aim to understand how Th17 cells exert pathological effects on brain development and subsequent behavioral changes in developing pups. In addition, they are investigating which fetal brain regions mediate the behavioral changes induced by immune mediators. They plan to look for gene expression changes in those areas.

This research may lead to the identification of biomarkers to predict autism-like behaviors in affected children, or to the development of therapeutic strategies to treat those behaviors by modulating Th17 cell function.