Plasmacytoid dendritic cell deficiency in neonates enhances allergic airway inflammation via reduced production of IFN- α.

We report here that this pDC deficiency renders neonatal mice more susceptible to severe allergic airway inflammation than adult mice in an OVA-induced experimental asthma model. Adoptive transfer of pDCs or administration of IFN-α to neonatal mice prevented the development of allergic inflammation in wild type but not in IFNAR1-/- mice. Similarly, adult mice developed more severe allergic inflammation when pDCs were depleted. The protective effects of pDCs were mediated by the pDC-/IFN-α-mediated negative regulation of the secretion of epithelial cell-derived CCL20, GM-CSF, and IL-33, which in turn impaired the recruitment of cDC2 and ILC2 cells to the airway. In asthmatic patients, the percentage of pDCs and the level of IFN-α were lower in children than in adults. These results indicate that impairment of pDC-epithelial cell crosstalk in neonates is a susceptibility factor for the development of allergen-induced allergic airway inflammation.
PMID: 31853001 [PubMed - as supplied by publisher]

Source: Cellular and Molecular Immunology - December 17, 2019 Category: Molecular Biology Authors: Wu M, Gao L, He M, Liu H, Jiang H, Shi K, Shang R, Liu B, Gao S, Chen H, Gong F, Gelfand EW, Huang Y, Han J Tags: Cell Mol Immunol Source Type: research