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,
* Division of Allergy and Immunology or
Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, and
Department of Cell Biology, Washington University School of Medicine, St. Louis, MO 63110
Dendritic cells are ideally suited to orchestrate the innate and adaptive immune responses to infection, but we know little about how these cells respond to infection with common respiratory viruses. Paramyxoviral infections are the most frequent cause of serious respiratory illness in childhood and are associated with an increased risk of asthma. We therefore used a high-fidelity mouse model of paramyxoviral respiratory infection triggered by Sendai virus to examine the response of conventional and plasmacytoid dendritic cells (cDCs and pDCs, respectively) in the lung. We found that pDCs are scarce at baseline but become the predominant population of lung dendritic cells during infection. This recruitment allows for a source of IFN-
locally at the site of infection. In contrast, cDCs rapidly differentiate into myeloid cDCs and begin to migrate from the lung to draining lymph nodes within 2 h after viral inoculation. These events cause the number of lung cDCs to decrease rapidly and remain decreased at the site of viral infection. Maturation and migration of lung cDCs depends on Ccl5 and Ccr5 signals because these events are significantly impaired in Ccl5–/– and Ccr5–/– mice. cDCs failure to migrate to draining lymph nodes in Ccl5–/– or Ccr5–/– mice is associated with impaired up-regulation of CCR7 that would normally direct this process. Our results indicate that pDCs and cDCs respond distinctly to respiratory paramyxoviral infection with patterns of movement that should serve to coordinate the innate and adaptive immune responses, respectively.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by an interest section grant from the American Academy of Asthma, Allergy, and Immunology, as well as grants from the National Institute of Allergy and Infectious Diseases and National Heart, Lung, and Blood Institute.
2 Address correspondence and reprint requests to Dr. Mitchell H. Grayson, Campus Box 8122, 660 South Euclid Avenue, Saint Louis, MO 63110. E-mail address: wheeze{at}allergist.com
3 Abbreviations used in this paper: RSV, respiratory syncytial virus; DC, dendritic cell; cDC, conventional DC; pDC, plasmacytoid DC; MHC-II, MHC class II; SeV, Sendai virus; i.n., intranasal(ly); PI, postinoculation.
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