These observations let the authors conclude that the presence of cord blood IgE was, in the majority of cases, a result of maternal transfer. Our results PI3K inhibitor showed a strong correlation between cord blood anti-Der p IgG, IgG1, IgG2 and IgG4 and respective maternal levels. Although we do not have data on IgG levels in children at 6 months of age, our data suggest a maternal transfer of anti-Der p IgG subclasses

across placenta. In addition, the decreased ratio of cord blood to maternal levels of these antibodies at high maternal concentrations suggests a saturable receptor-mediated transfer. Notably, the syncytiotrophoblast expresses a neonatal Fc receptor (FcRn) that is essential for IgG transfer [3, 39] and is saturable [40]. This receptor has a higher affinity for IgG1, compared to other IgG subclasses, which may explain the more efficient in utero transfer of Der p-specific IgG1, compared to other subclasses [3], as also shown here. Several studies in rodents have reported that maternal allergen-specific IgG inhibits allergic responses in the offspring [2, 9–16]. Proposed mechanisms of protection by maternal IgG include the following: (1) IgG binding to allergen, leading to allergenic determinant masking and clearance of the immune complexes by phagocytosis,

(2) IgG blockade of IgE binding to allergen and hence inhibition of mast cell degranulation and (3) interactions with inhibitory receptor FcγRIIb on neonatal B lymphocytes or dendritic cells [2, 41]. More recently, protection from allergic airway disease Clomifene by antigen transfer Selleck Temsirolimus through breast milk was shown to be more stronger and of longer duration when maternal allergen-specific IgG is present in breast milk. The authors attributed the increased protection to the formation of allergen–IgG immune complexes that are easily transferred across the neonatal gut barrier compared to uncomplexed antigen and display tolerogenic properties [42]. Human studies also suggest an immunoregulatory role for in utero transfer of maternal IgG. A study by Glovsky et al. [43] analysed the effect of specific immunotherapy during pregnancy on allergic sensitization in

children. Their data suggested that blocking antibodies induced by immunotherapy were transferred across the placenta and were responsible for decreased allergic sensitization in their children. Jenmalm and Bjorkstén [21] found that high concentration of IgG directed to inhaled allergens in cord blood was associated with reduced atopy in children. Another study showed a transient protective effect of placental transfer of maternal antibodies on allergic immune response [22]. The current study demonstrated a higher concentration of specific IgG4 and, to a lesser extent, of IgG2 in cord blood of neonates from atopic mothers compared to non-atopic mothers. Although we cannot conclude that these IgG subclasses exert an immunoregulatory role, a protective effect has previously been reported for IgG4 [44–46].