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Summary   Background  The mechanism(s) responsible for acquisition of maternal antibody isotypes other than IgG are not fully understood. This uncertainty is a major reason underlying the continued controversy regarding whether cord blood ( CB ) IgE originates in the mother or fetus.    Objective  To investigate the capacity of maternal IgE to be transported across the placenta in the form of IgG anti‐IgE/IgE immune complexes ( IC s) and to determine the role of the neonatal Fc receptor (FcRn) in mediating this process.    Methods  Maternal and  CB  serum concentrations of IgE, IgG anti‐IgE, and IgG anti‐IgE/IgE  IC s were determined in a cohort of allergic and non‐allergic mother/infant dyads. Madin–Darby canine kidney ( MDCK ) cells stably transfected with human FcRn were used to study the binding and transcytosis of IgE in the form of IgG anti‐IgE/IgE  IC s.    Results  Maternal and  CB  serum concentrations of IgG anti‐IgE/IgE  IC s were highly correlated, regardless of maternal allergic status. IgG anti‐IgE/IgE  IC s generated  in vitro  bound strongly to FcRn‐expressing  MDCK  cells and were transcytosed in an FcRn‐dependent manner. Conversely, monomeric IgE did not bind to FcRn and was not transcytosed. IgE was detected in solutions of transcytosed IgG anti‐IgE/IgE  IC s, even though essentially all the IgE remained in complex form. Similarly, the majority of IgE in  CB  sera was found to be complexed to IgG.    Conclusions and Clinical Relevance  These data indicate that human FcRn facilitates the transepithelial transport of IgE in the form of IgG anti‐IgE/IgE  IC s. They also strongly suggest that the majority of IgE in  CB  sera is the result of FcRn‐mediated transcytosis of maternal‐derived IgG anti‐IgE/IgE  IC s. These findings challenge the widespread perception that maternal IgE does not cross the placenta. Measuring maternal or  CB  levels of IgG anti‐IgE/IgE  IC s may be a more accurate predictor of allergic risk.

Evidence that F c R n mediates the transplacental passage of maternal IgE in the form of I g G anti‐ I g E / I g E immune complexes