Figure 1: Proposed role of resident lung dendritic cells in the development of postviral atopic disease. After infection with a respiratory virus, both conventional (green cell) and plasmacytoid (tan cell) dendritic cells can influence the development of atopy. Conventional dendritic cells (cDCs) are able to present antigen to naïve T cells and skew their development towards a Th2 lineage (purple cell being converted to the blue cell). In addition, in a type I IFN-dependent fashion, CD49d-expressing neutrophils are recruited to the airway during the infection. These cells induce FcεRI expression on lung cDC, which can be bound by anti-viral IgE. Subsequent cross-linking of the anti-viral IgE by virus leads to the production of CCL28, which further recruits Th2 cells to the airway, leading to atopic disease. The plasmacytoid dendritic cell (pDC) is induced to produce IFN-α by the viral infection through toll-like receptors (TLRs). The IFN-α blocks the development of atopy. Whether this type I IFN drives the CD49d+ neutrophil response is not known (the dotted line). Similar to the cDC, anti-viral IgE can bind FcεRI on the pDC, with the free virus cross-linking the receptor. This impairs the release of IFN-α from the TLR removing the pDC-mediated inhibition of postviral atopic disease. See text for more details.