Fetal development is largely dependent on the mother. However, pregnancy maintenance and consequently fetal development are highly vulnerable and sensitive to disruption, triggered by, for example, prenatal stress challenge. Such prenatal stress challenge modulates the maternal endocrine and immune responses during pregnancy e.g. by decreasing levels of progesterone. Prenatal stress also has negative repercussions for the child's health later in life. It has been reported that prenatal stress increases the risk of the child to develop chronic immune diseases such as allergies and asthma. We therefore propose that prenatal stress challenge - associated with a decrease in maternal progesterone - impairs fetal immune development (immune ontogeny). Such impaired immune ontogeny carries over into postnatal life, rendering the child more prone to developing chronic immune diseases. This purported association urgently requires a fresh evaluation in order to identify biomarkers and cascades of events. In the present review, we outline candidate biomarkers involved in fetal immune ontogeny, which may be targets of prenatal stress challenge and subsequently determine offspring disease risk. Identification of these stress-sensitive biomarkers may allow detection of pregnant women at risk to deliver chronic immune disease-prone offspring. The creation of therapeutic interventions designed to prevent negative consequences of prenatal stress would then be within reach.
