Journal
IMMUNITY
Volume 45, Issue 6, Pages 1285-1298Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2016.10.031
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Funding
- VENI grant of the Dutch Scientific Organization (NWO)
- Long-term Fellowship grant European Respiratory Society - Marie Curie
- Long-term Fellowship grant European Respiratory Society - Intra-European Fellowship Grant of Marie Curie (IEF-FP7)
- FWO project grant
- ERC consolidator grant [261231]
- University of Gent MRP grant (GROUP-ID consortium)
- FP7 (MedAll) grant
- IMI (UBiopred) grant
- Lung Foundation Netherlands [3.2.12.067, 5.1.14.020]
- European Research Council (ERC) [261231] Funding Source: European Research Council (ERC)
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Allergic disease originates in early life and polymorphisms in interleukin-33 gene (IL33) and IL1RL1, coding for IL-33R and decoy receptor sST2, confer allergy risk. Early life T helper 2 (Th2) cell skewing and allergy susceptibility are often seen as remnants of feto-maternal symbiosis. Here we report that shortly after birth, innate lymphoid type 2 cells (ILC2s), eosinophils, basophils, and mast cells spontaneously accumulated in developing lungs in an IL-33-dependent manner. During the phase of postnatal lung alveolarization, house dust mite exposure further increased IL-33, which boosted cytokine production in ILC2s and activated CD11b(+) dendritic cells (DCs). IL-33 suppressed IL-12p35 and induced OX40L in neonatal DCs, thus promoting Th2 cell skewing. Decoy sST2 had a strong preventive effect on asthma in the neonatal period, less so in adulthood. Thus, enhanced neonatal Th2 cell skewing to inhaled allergens results from postnatal hyperactivity of the IL-33 axis during a period of maximal lung remodeling.
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