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Journal of Virology, May 2008, p. 4908-4919, Vol. 82, No. 10
0022-538X/08/$08.00+0     doi:10.1128/JVI.02367-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Differential Response of Respiratory Dendritic Cell Subsets to Influenza Virus Infection{triangledown}

Xueli Hao,1,2 Taeg S. Kim,1 and Thomas J. Braciale1,2,3*

The Carter Immunology Center,1 Department of Pathology,2 Department of Microbiology, University of Virginia Health Sciences Center, Charlottesville, Virginia 229083

Received 1 November 2007/ Accepted 26 February 2008

Dendritic cells (DC) are believed to play an important role in the initiation of innate and adaptive immune responses to infection, including respiratory tract infections, where respiratory DC (RDC) perform this role. In this report, we examined the susceptibilities of isolated murine RDC to influenza virus infection in vitro and the effect of the multiplicity of infection (MOI) on costimulatory ligand upregulation and inflammatory cytokine/chemokine production after infection. We found that the efficiency of influenza virus infection of RDC increased with increasing MOIs. Furthermore, distinct subpopulations of RDC differed in their susceptibilities to influenza virus infection and in the magnitude/tempo of costimulatory ligand expression. Additional characterization of the CD11c-positive (CD11c+) RDC revealed that the identifiable subsets of RDC differed in susceptibility to infection, with CD11c+ CD103+ DC exhibiting the greatest susceptibility, CD11c+ CD11bhi DC exhibiting intermediate susceptibility, and CD11c+ B220+ plasmacytoid DC (pDC) exhibiting the least susceptibility to infection. A companion analysis of the in vivo susceptibilities of these RDC subsets to influenza virus revealed a corresponding infection pattern. The three RDC subsets displayed different patterns of cytokine/chemokine production in response to influenza virus infection in vitro: pDC were the predominant producers of most cytokines examined, while CD103+ DC and CD11bhi DC produced elevated levels of the murine chemokine CXCL1 (KC), interleukin 12p40, and RANTES in response to influenza virus infection. Our results indicate that RDC are targets of influenza virus infection and that distinct RDC subsets differ in their susceptibilities and responses to infection.

* Corresponding author. Mailing address: Carter Immunology Center, UVA, P.O. Box 801386, Charlottesville, VA 22908. Phone: (434) 924-1219. Fax: (434) 924 1221. E-mail: tjb2r{at}virginia.edu

{triangledown} Published ahead of print on 19 March 2008.

Journal of Virology, May 2008, p. 4908-4919, Vol. 82, No. 10
0022-538X/08/$08.00+0     doi:10.1128/JVI.02367-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



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