CD49d+ neutrophils induce FcεRI expression on lung dendritic cells in a mouse model of postviral asthma

The increasing prevalence of atopy and asthma remains unexplained but may be due to infection with respiratory viruses. In support of this hypothesis, we showed that experimental asthma after viral infection in mice depended on type I IFN-driven up-regulation of the high-affinity receptor for IgE (FceRI) on conventional dendritic cells (cDCs) in the lung. Here we demonstrate that FceRI expression on lung cDCs depends on an unexpected activity of a CD49d+ subset of polymorphonuclear neutrophils (PMNs) that are found in the lungs of wild-type C57BL6 but not IFNAR−/− mice. Expression of FceRI depends in part on a CD11b-dependent interaction between PMNs and cDCs. This study demonstrates a novel PMN-cDC interaction in the lung that is necessary for the ability of viral infection to induce atopic disease.