The managed immune system: protecting the womb to delay the tomb.

The developing immune system serves as a novel target for disruption by environmental chemicals and drugs, and one that can significantly influence later-life health risks. Specific immune maturational events occur during critical windows of pre- and early postnatal development that are not effectively modeled using adult exposure-assessment or general developmental toxicity screens. The range of postnatal health risks linked to developmental immunotoxicity (DIT) is influenced, in part, by the natural progression of prenatal-neonatal development. In this progression, the pregnancy itself imposes a Th2-bias in utero, and this produces a delay in the acquisition of Th1 functional capacity in the newborn. The status of Th1 regulatory and Th17 populations may also be important in immune function/dysfunction considerations. The necessary shift from a Th2 preferred capacity in late gestation to a more balance functional capacity in the neonate can be disrupted by xenobiotics leaving the child with increased vulnerability to a range of potential diseases. Knowledge of environmental factors that facilitate effective immune functional maturation as well as those xenobiotics capable of disrupting the process is important in strategies to reduce the incidence of diseases such as childhood asthma. Because hormesis has been shown to be an important factor in modulation of the adult immune system, it becomes even more important to understand potentially opposing dose-response effects for the immune system of the fetus, neonate, and juvenile. The direct linkage between immune dysfunction and chronic disease has become abundantly apparent in recent years. Therefore, a more comprehensive and effective approach for the protection of the developing immune system can help to reduce the incidence of later-life chronic diseases.