Maternal influences on offspring food allergy

Abstract

The prevalence of allergies has been globally escalating. While allergies could appear at any age, they often develop in early life. However, the significant knowledge gap in the field is the mechanisms by which allergies affect certain people but not others. Investigating early factors and events in neonatal life that have a lasting impact on determining the susceptibilities of children to develop allergies is a significant area of the investigation as it promotes the understanding of neonatal immune system that mediates tolerance versus allergies. This review focuses on the research over the recent 10 years regarding the potential maternal factors that influence offspring allergies with a view to food allergy, a potentially life-threatening cause of anaphylaxis. The role of breast milk, maternal diet, maternal antibodies, and microbiota that have been suggested as key maternal factors regulating offspring allergies are discussed here. We also suggest future research area to expand our knowledge of maternal-offspring interactions on the pathogenesis of food allergy.

Keywords: antibodies; breast milk; food allergy; immune complex microbiota.

Figure 1.. Potential mechanisms of maternal influences on offspring FA.

Breast milk contains immunoactive components including Ig, cytokines, microbiota, and HMOs that shape the offspring’s immune system. Maternal food allergen-specific IgG binds to food allergen and forms IgG-IC that appear in breast milk. Maternal IgG-IC in milk were transferred and presented by CD11c⁺ cells in offspring in FcRn-dependent manner. This resulted in the induction of allergen-specific Foxp3⁺ Treg cells that suppressed FA , indicating that maternal milk IgG-IC-FcRn axis establishes Treg cell-mediated neonatal food tolerance, which may extend to humans. This pathway of protection may be mediated by additional milk factors such as microbiota and HMOs, which facilitate the development of microbiota-induced Rorγt⁺ Treg cells. The potential mechanisms include colonization with tolerogenic bacteria, enhancement of intestinal permeability, and maturation of immune cells.