Maternal Immunization and Allergy Development Mechanisms

Maternal immunization represents a promising strategy to steer offspring immune development away from allergic sensitisation by transferring antigen‐specific immune factors during pregnancy and lactation. Protective maternal antibodies, cytokines and antigen complexes traverse the placenta or are delivered via breast milk to influence the neonatal immune milieu. These maternal immunomodulators can induce regulatory B and T cell populations, alter inhibitory and activating receptor expression on lymphocytes and shape thymic maturation pathways. Key mechanisms include the upregulation of the inhibitory FcγRIIB receptor on B cells, the generation of IL-10‐producing regulatory B10 cells, modulation of γδ T-cell cytokine profiles and imprinting of innate lymphoid cell subsets. Collectively, these processes recalibrate the balance of type 1 and type 2 immunity in early life, reducing IgE responses, dampening Th2 cytokine production and promoting long-term tolerance to common allergens. Translating these insights into maternal vaccine strategies holds potential for global reduction of paediatric allergic disease.

Research from Nature Portfolio

Recent studies have demonstrated that polyclonal IgG from individuals allergic to the house-dust mite Dermatophagoides pteronyssinus directly interacts with human neonatal thymic B cells to modulate their homing receptors and cytokine secretion. Allergen-specific IgG was shown to suppress pro-inflammatory IFN-γ and IL-9 production while enhancing IL-10-producing B cells. These findings reveal a mechanism by which maternal or adult atopic antibody repertoires can reprogramme central B-cell tolerance and potentially predispose or protect the offspring against allergic outcomes.

Maternal Immunization and Allergy Development Mechanisms publication trend

The graph below shows the total number of articles in maternal immunization and allergy development mechanisms across all publications each year (not limited to Nature Index journals).

Technical terms

FcγRIIB: An inhibitory receptor on B cells that attenuates B-cell receptor signalling to prevent excessive antibody responses.

B10 cells: A subset of regulatory B cells characterised by their production of the anti-inflammatory cytokine IL-10, which contributes to immune tolerance.

γδ T cells: Non-conventional T lymphocytes bearing a γδ T-cell receptor, involved in early innate-like immune responses and tissue homeostasis.

ILC2: Group 2 innate lymphoid cells that secrete type 2 cytokines such as IL-5 and IL-13, playing key roles in allergic inflammation and tissue repair.

References

1. IgG from Dermatophagoides pteronyssinus (Der p)-atopic individuals modulates non-atopic thymic B cell phenotype (alfa-4/beta-7) and cytokine production (IFN-γ, IL-9, and IL-10) with direct membrane interaction. Scientific Reports (2024).
2. Preconception allergen sensitization can induce B10 cells in offspring: a potential main role for maternal IgG. Allergy, Asthma & Clinical Immunology (2017).
3. Maternal immunization with ovalbumin prevents neonatal allergy development and up-regulates inhibitory receptor FcγRIIB expression on B cells. BMC Immunology (2010).
4. IgG from Adult Atopic Dermatitis (AD) Patients Induces Nonatopic Neonatal Thymic Gamma–Delta T Cells (γδT) to Acquire IL-22/IL-17 Secretion Profile with Skin-Homing Properties and Epigenetic Implications Mediated by miRNA. International Journal of Molecular Sciences (2022).
5. Non-atopic Neonatal Thymic Innate Lymphoid Cell Subsets (ILC1, ILC2, and ILC3) Identification and the Modulatory Effect of IgG From Dermatophagoides Pteronyssinus (Derp)-Atopic Individuals. Frontiers in Allergy (2021).