Our analysis of maternal T cell populations within fetal tissues did not support this conclusion, however, and subsequent experiments demonstrated that the increased incidence of stillbirth more likely resulted from reexposure of the primed maternal immune system to AAV antigen resulting in a systemic maternal inflammatory response characterized by elevated IL-6 and CXCL1 and affecting the placenta. This evidence concerns the gene CXCL1 and Stillbirth.