Programming for responsiveness to environmental antigens that trigger allergic respiratory disease in adulthood is initiated during the perinatal period.

Allergy to airborne environmental antigens (allergens) is a major cause of asthma in children and adults. This review argues that the development of allergen-specific immunologic memory of the type that predisposes to allergy development is the end result of a T-cell selection process operative during infancy, which is triggered via encounters between the immature immune system and incoming airborne allergens from the environment. In normal individuals this process leads to the development of allergen-specific T-memory cells that secure the T helper (Th)-1 pattern of cytokines, which actively suppress the growth of their allergy-inducing Th-2 cytokine-secreting counterparts. However, these protective allergen-reactive Th-1 memory cells fail to develop in some individuals, permitting the subsequent proliferation of allergen-specific Th-2 cells that can trigger allergic reactions. Recent evidence suggests that genetic predisposition to allergy may be due in part to hyperactivity of control mechanisms operative in utero and which normally protect the fetoplacental unit against the toxic effect of Th-1 cytokines.