Cutting edge: CD49d+ neutrophils induce FcepsilonRI expression on lung dendritic cells in a mouse model of postviral asthma. J Immunol 2010 Nov 01;185(9):4983-7
Date
09/30/2010Pubmed ID
20876348Pubmed Central ID
PMC2959147DOI
10.4049/jimmunol.1002456Scopus ID
2-s2.0-78149481931 (requires institutional sign-in at Scopus site) 53 CitationsAbstract
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 upregulation of FcεRI on conventional dendritic cells (cDCs) in the lung. In this article, we demonstrate that FcεRI 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 mice deficient in type I IFNR. Expression of FcεRI depends in part on a CD11b-dependent interaction between PMNs and cDCs. This study demonstrates a PMN-cDC interaction in the lung that is necessary for the ability of viral infection to induce atopic disease.
Author List
Cheung DS, Ehlenbach SJ, Kitchens RT, Riley DA, Thomas LL, Holtzman MJ, Grayson MHMESH terms used to index this publication - Major topics in bold
AnimalsAsthma
Cell Separation
Cells, Cultured
Dendritic Cells
Disease Models, Animal
Flow Cytometry
Immunohistochemistry
Integrin alpha4
Lung
Mice
Mice, Inbred C57BL
Mice, Knockout
Neutrophils
Receptor, Interferon alpha-beta
Receptors, IgE
Respiratory Tract Infections
Respirovirus Infections
Reverse Transcriptase Polymerase Chain Reaction
Sendai virus
