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Journal of Virology, February 2005, p. 2432-2439, Vol. 79, No. 4
0022-538X/05/$08.00+0 doi:10.1128/JVI.79.4.2432-2439.2005
Differential Effects of Dengue Virus on Infected and Bystander Dendritic Cells
Dupeh R. Palmer,1,
Peifang Sun,2,
Christina Celluzzi,3
John Bisbing,1
Somnang Pang,1
Wellington Sun,1
Mary A. Marovich,4 and
Timothy Burgess2*
Department of Viral Diseases, Walter Reed Army Institute of Research,1
Viral Diseases Department, Naval Medical Research Center, Silver Spring,2
Blood and Cell Therapy Development, Holland Laboratory, American Red Cross,3
Henry M. Jackson Foundation, Rockville, Maryland4
Received 1 July 2004/
Accepted 27 August 2004
Dendritic cells (DCs) play a central role as major targets of dengue virus (DV) infections and initiators of antiviral immune responses. Previous observations showed that DCs are activated by infection, presumably acquiring the capacity to promote cell-mediated immunity. However, separate evaluations of the maturation profiles of infected and uninfected bystander cells show that infection impairs the ability of DCs to upregulate cell surface expression of costimulatory, maturation, and major histocompatibility complex molecules, resulting in reduced T-cell stimulatory capacity. Infected DCs failed to respond to tumor necrosis factor alpha as an additional maturation stimulus and were apoptotic. Interleukin 10 (IL-10) was detected in supernatants from cultures of DV-infected DCs and cocultures of DCs and T cells. Taken together, these results constitute an immune evasion strategy used by DV that directly impairs antigen-presenting cell function by maturation blockade and induction of apoptosis.
* Corresponding author. Mailing address: Naval Medical Research Center, 503 Robert Grant Ave., Silver Spring, MD 20910. Phone: (301) 319-7688. Fax: (301) 319-7451. E-mail: BurgessT{at}NMRC.navy.mil.
D.R.P. and P.S. contributed equally to this work.
Journal of Virology, February 2005, p. 2432-2439, Vol. 79, No. 4
0022-538X/05/$08.00+0 doi:10.1128/JVI.79.4.2432-2439.2005
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