Abstract
AbstractPrenatal imprinting to interleukin 17A (IL-17A) triggers behavioral disorders in offspring, but reported models lack specificity to elucidate the side of its action and the precise abnormalities it causes. By combining transgenic IL-17A overexpression with maternal deficiency in the receptor for IL-17A, we established a novel model to study embryo-restricted IL-17A responses. We demonstrated IL-17A transfer across the placental barrier and subsequent development of selected behavioral deficits in mouse offspring.
Publisher
Cold Spring Harbor Laboratory