The Journal of Experimental Medicine
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Published online October 22, 2007
doi:10.1084/jem.20070360
The Journal of Experimental Medicine, Vol. 204, No. 11, 2759-2769
The Rockefeller University Press, 0022-1007 $30.00
© 2007 Grayson et al.
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ARTICLE

 Induction of high-affinity IgE receptor on lung dendritic cells during viral infection leads to mucous cell metaplasia

Mitchell H. Grayson1, Dorothy Cheung1, Michelle M. Rohlfing1, Robert Kitchens1, Daniel E. Spiegel1, Jennifer Tucker2, John T. Battaile2, Yael Alevy2, Le Yan2, Eugene Agapov2, Edy Y. Kim2, and Michael J. Holtzman2,3

1 Division of Allergy and Immunology, 2 Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, and 3 Department of Cell Biology, Washington University School of Medicine, Saint Louis, MO 63110

CORRESPONDENCE Mitchell H. Grayson:wheeze{at}allergist.com

Respiratory viral infections are associated with an increased risk of asthma, but how acute Th1 antiviral immune responses lead to chronic inflammatory Th2 disease remains undefined. We define a novel pathway that links transient viral infection to chronic lung disease with dendritic cell (DC) expression of the high-affinity IgE receptor (Fc{epsilon}RI{alpha}). In a mouse model of virus-induced chronic lung disease, in which Sendai virus triggered a switch to persistent mucous cell metaplasia and airway hyperreactivity after clearance of replicating virus, we found that FceRIa–/– mice no longer developed mucous cell metaplasia. Viral infection induced IgE-independent, type I IFN receptor–dependent expression of Fc{epsilon}RI{alpha} on mouse lung DCs. Cross-linking DC Fc{epsilon}RI{alpha} resulted in the production of the T cell chemoattractant CCL28. FceRIa–/– mice had decreased CCL28 and recruitment of IL-13–producing CD4+ T cells to the lung after viral infection. Transfer of wild-type DCs to FceRIa–/– mice restored these events, whereas blockade of CCL28 inhibited mucous cell metaplasia. Therefore, lung DC expression of Fc{epsilon}RI{alpha} is part of the antiviral response that recruits CD4+ T cells and drives mucous cell metaplasia, thus linking antiviral responses to allergic/asthmatic Th2 responses.

Abbreviations used: ATCC, American Type Culture Collection; IFNAR, type I IFN receptor; PI, postinnoculation; SeV, Sendai virus.


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