Transfer of maternal immunity and programming of the newborn immune system

Abstract

As placental mammals, the pregnant women and the fetus have intense and prolonged interactions during gestation. There is increasing evidence that multiple molecular as well as cellular components originating in pregnant women are transferred to the fetus. The transfer of maternal antibodies has long been recognized as a central component of newborn immunity against pathogens. More recent studies indicate that inflammatory mediators, micronutrients, microbial products and maternal cells are transferred in utero and influence the fetal immune system. Together, these multiple signals are likely to form a complex network of interactions that program the neonatal immune system and tune its homeostatic regulation. Maternal disorders, in particular infectious diseases, modify these signals and may thereby alter immunity in early life. Understanding maternal programming of the newborn immune system could provide a basis for interventions promoting child health.

Immunobiological aspects of vaccines in pregnancy: Maternal perspective

“…As the FcRn is not expressed by fetal endothelial cells, other receptors have to participate in the transport of IgG to the fetal circulation. Studies suggest that the FcγRIIb2 expressed by fetal endothelial cells could be involved but its role in maternal antibody transfer is still debated [110,111]. A better understanding of the molecular and cellular basis of maternal antibody transfer across the placenta would help designing vaccines inducing antibodies with optimal transferability to the fetus.…”

Role of early life immune regulation in asthma development

“…They form a complex network of multiple signals that provide immunity, program the neonatal immune system, and modulate its homeostatic regulation. There is even increasing evidence that allergens and microbial antigens can cross the placenta [8]. After birth, the newborn's immunity has to adapt to the altered circumstances rapidly.…”

“…Since maternal IgG is transferred across the placenta, neonatal IgG levels are remarkably high at birth but decrease within the first 3 months due to metabolization of maternal IgG before IgG production starts, resulting in a physiological hypogammaglobulinemia of infancy [26]. At birth, there are also low serum levels of IgE and IgA [8]. IgE might be transferred to the fetus as IgG/IgE complexes [8].…”

“…At birth, there are also low serum levels of IgE and IgA [8]. IgE might be transferred to the fetus as IgG/IgE complexes [8]. The breastfed infant also receives IgA and IgM transferred by polymeric immunoglobulin receptors across mammary epithelial cells [8].…”

Immunity and immunopathology in early human life

“…The concept of functional fetal adaptive immune responses is further explored by the group around Richard Lo-Man, presenting evidence of in utero development of memory T cells [8], while Donna Farber and colleagues place this early life T cell development into the context of tissue compartmentalization [9]. These pre-natal immune events clearly do not happen in isolation, but are modulated by the maternal immune system, as reviewed by Arnaud Marchant's group [10]. The impact of such pre-and perinatal events on neonatal infection then is examined by Tobias Kollmann's team [11], while Beate Kampmann and colleagues focus on this impact in regard to neonatal vaccination [12].…”