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Plasmacytoid Dendritic Cells Are Dispensable during Primary Influenza Virus Infection¹

Amaya I. Wolf^*, Darya Buehler^*, Scott E. Hensley, Lois L. Cavanagh^*,, E. John Wherry^*, Philippe Kastner, Susan Chan and Wolfgang Weninger^2,*,,¶

^* Immunology Program, The Wistar Institute, Philadelphia, PA 19104; National Institutes of Health/National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892; Institut de Genetique et de Biologie Molculaire et Cellulaire, Illkirch CU Strasbourg, France; The Centenary Institute for Cancer Medicine and Cell Biology, Newtown, New South Wales, Australia; and ^¶ Discipline of Dermatology, University of Sydney, Camperdown, New South Wales, Australia

Plasmacytoid dendritic cells (pDC) are thought to be pivotal in the first line of defense against viral infections. Although previous studies have suggested that pDC regulate the immune response against respiratory syncytial virus, their role in pulmonary infection with influenza virus has remained unclear. Using mice with GFP-tagged pDC, we observed a marked increase in pDC numbers in the lung airways 3 days after intranasal infection with influenza virus A/PR/8/34. To further investigate their potential involvement in the disease, we made use of pDC-deficient Ikaros^L/L mice. In the absence of pDC, the recruitment of T cells to the bronchoalveolar space was delayed, which could be reversed by the adoptive transfer of pDC before infection. Surprisingly, however, when compared with wild-type animals, Ikaros^L/L mice revealed a similar course of disease, as determined by weight loss, viral titers, levels of neutralizing Ab, and lung pathology. Moreover, the activation and differentiation of influenza-specific CD8⁺ effector T cells was unaltered in the absence of pDC, as was the generation of CD8⁺ memory T cells. Taken together, our study suggests that pDC regulate the accumulation of T cells in the bronchoalveolar space during early influenza virus infection, but are dispensable for the control of this disease.

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 a Special Population contract from the National Institutes of Health, National Health and Medical Research Council Grant 512266 and a Life Sciences Award from the New South Wales government.

² Address correspondence and reprint requests to Dr. Wolfgang Weninger, The Centenary Institute, Locked Bag. No. 6, Newtown, NSW 2042, Australia. E-mail address: w.weninger{at}centenary.org.au

³ Abbreviations used in this paper: DC, dendritic cell; mDC, myeloid DC; pDC, plasmacytoid DC; RSV, respiratory syncytial virus; MCMV, murine cytomegalo virus; DPE^GFP, transgenic mice expressing GFP under the distal and proximal CD4 enhancer and promoter elements; LCMV, lymphocytic choriomeningitis virus; BAL, bronchoalveolar lavage; BM, bone marrow; LN, lymph node; medLN, mediastinal lymph node.

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