Several studies provide indirect evidence that already the prenatal environment plays an important and decisive role for the development of allergy later in life. Since the underlying mechanisms still remain unclear, we established a murine model of prenatal allergen-sensitization and/or allergen-exposure to study the impact of maternal allergy on the development of an allergic immune response in early life.

An allergic TH-2 response was induced in pregnant mice by sensitization and aerosol allergen exposure.

Both, IgG1 and IgG2a, but not IgE antibodies cross the placental barrier. Free allergen also crosses the placental area and was detected in serum and amniotic fluids of neonatal F1 mice. These F1 mice demonstrated a suppressed TH-1 response as reflected by lowered frequencies and reduced levels of IFN- production. Development of an IgE response against the same allergen was completely prevented early in life. This effect was mediated by diaplacental transfer of allergen-specific IgG1 antibodies. In contrast, allergic sensitization against a different allergen early in life was accelerated in these mice. This effect was mediated by maternal CD4 and OVA-specific TH-2 cells induced by allergic sensitization during pregnancy.

These data indicate a critical role for maternal adaptive immune response in shaping pre- and postnatal development of an allergic immune response.