Prenatal Contact with Inhalant Allergens

Abstract

Pollen contact in early infancy may enhance the risk for subsequent pollen allergy. In this study likelihood of a prenatal antigen contact, as a result of inhalation of pollen allergens by the mother, was investigated. Due to the seasonal occurrence of allergens studied, the date of priming can be estimated, and this can supply data about the maturation of the fetal immune system. Proliferative responses of umbilical cord blood mononuclear cells (UCB MNCs) to the recombinant major allergens of birch (rBet v 1) and timothy grass (rPhl p 1) were analyzed throughout the whole year. A positive proliferative response was regarded as the criterion for a prenatal contact of the immune system with the allergen. Prenatal priming with both allergens was observed. Timothy grass pollen displayed considerably higher antigenicity than did birch pollen. The susceptibility of the fetal immune system to be primed by these allergens varies during the gestation period. The majority of positive responses to rPhl p 1 and rBet v 1 were found in UCB samples in which antigen contact (the respective pollen season) took place in the first 6 mo of pregnancy. Our results offer indirect evidence that, shortly after migration of T cell precursors to the epithelial thymus, T cells are mature enough for priming with antigens. No relationship was found between the susceptibility of the fetal immune system to be primed by these allergens and the clinical history of the family concerning type I allergy.

Antibody Repertoire Development in Fetal And Neonatal Piglets. IV. Switch Recombination, Primarily in Fetal Thymus, Occurs Independent of Environmental Antigen and Is Only Weakly Associated with Repertoire Diversification

“…Although such cells could be of maternal origin, analysis of microsatellite DNA suggests that they are indeed of fetal origin (27). Responsive cells can be found even in the first 6 mo of pregnancy (29,30), suggesting that allergens may cross the placenta alone during this stage of pregnancy and do not require shuttle as IgG immune complexes. Thus, low-level stimulation of the human fetus by T-dependent Ags that cross the placenta alone or as immune complexes may account for any fetal switched isotypes found.…”

“…Unfortunately, the human fetus is a poor model because active transport of maternal IgG to the fetus progressively increases during the third trimester, and eventually concentrations in cord blood exceed maternal levels just before birth (24 -26). Furthermore, allergen-primed T cells can be found in the human fetus suggesting that allergens also can cross the placenta after they have been encountered by the pregnant mother either alone or as part of transported IgG immune complexes (27)(28)(29)(30). Although such cells could be of maternal origin, analysis of microsatellite DNA suggests that they are indeed of fetal origin (27).…”

Direct Evidence for Transplacental Allergen Transfer

“…The time at which maternofetal allergen exposure takes place in the course of a pregnancy is less clear. The current knowledge suggests early times during gestation, presumably around wk 20 of gestation (5,14), Szépfalusi et al unpublished experiments).…”

“…Allergen-specific T cell proliferation in cord blood cells has been demonstrated by many groups and for many different allergens (5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15). Inhalant and nutritive allergens in the form of crude extracts [birch pollen (5,7), house dust mite (8 -10, 15), timothy grass pollen (5, 7), cat fur (5, 7), BLG (5,7,13,16), alpha-casein (13), beta-casein (13), kappa-casein (13), BSA (5)(6)(7)13), and ovalbumin (5,7,11,15,16)] and in the form of recombinant allergens [Lol p1 (9), Der p1 (9), Bet v1 (14), and Phl p1 (14)] has been studied.…”

“…Inhalant and nutritive allergens in the form of crude extracts [birch pollen (5,7), house dust mite (8 -10, 15), timothy grass pollen (5, 7), cat fur (5, 7), BLG (5,7,13,16), alpha-casein (13), beta-casein (13), kappa-casein (13), BSA (5)(6)(7)13), and ovalbumin (5,7,11,15,16)] and in the form of recombinant allergens [Lol p1 (9), Der p1 (9), Bet v1 (14), and Phl p1 (14)] has been studied. A line of evidence now supports the hypothesis that fetal T cells are exposed during gestation to maternally derived allergens.…”