Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 215, Issue 1, Pages 91-113Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20171163
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Funding
- Food Allergy Research and Education (FARE)
- HOPEAPFED/ARTrust Pilot Grant
- William F. Milton Fund
- Harvard Catalyst Clinical and Translational Research Center (NCATS) [8UL 1TR000170]
- Boston Children's Hospital Pediatric Associates Award
- National Institutes of Health [DK053056]
- Harvard Digestive Diseases Center [P30DK034854]
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R56DK053056, P30DK034854, R01DK053056] Funding Source: NIH RePORTER
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The role of maternal immune responses in tolerance induction is poorly understood. To study whether maternal allergen sensitization affects offspring susceptibility to food allergy, we epicutaneously sensitized female mice with ovalbumin (OVA) followed by epicutaneous sensitization and oral challenge of their offspring with OVA. Maternal OVA sensitization prevented food anaphylaxis, OVA-specific IgE production, and intestinal mast cell expansion in offspring. This protection was mediated by neonatal crystallizable fragment receptor (FcRn)-dependent transfer of maternal IgG and OVA immune complexes (IgG-IC) via breast milk and induction of allergen-specific regulatory T (T reg) cells in offspring. Breastfeeding by OVA-sensitized mothers or maternal supplementation with IgG-IC was sufficient to induce neonatal tolerance. FcRn-dependent antigen presentation by CD11c(+) dendritic cells (DCs) in offspring was required for oral tolerance. Human breast milk containing OVA-IgG-IC induced tolerance in humanized FcRn mice. Collectively, we demonstrate that interactions of maternal IgG-IC and offspring FcRn are critical for induction of T reg cell responses and control of food-specific tolerance in neonates.
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