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Journal of Virology, May 2004, p. 5223-5232, Vol. 78, No. 10
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.10.5223-5232.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Human Immunodeficiency Virus Type 1 Activates Plasmacytoid Dendritic Cells and Concomitantly Induces the Bystander Maturation of Myeloid Dendritic Cells

Jean-François Fonteneau,1,{dagger} Marie Larsson,2,{dagger} Anne-Sophie Beignon,2 Kelli McKenna,2 Ida Dasilva,2 Ali Amara,3 Yong-Jun Liu,4 Jeffrey D. Lifson,5 Dan R. Littman,3 and Nina Bhardwaj2*

Institut de Biologie, INSERM U463, Nantes, France,1 Departments of Medicine and Pathology,2 Howard Hughes Medical Institute and Molecular Pathogenesis Program, Skirball Institute of Biomolecular Medicine, New York University School of Medicine, New York, New York,3 Department of Immunology and Center for Cancer Immunology Research, MD Anderson Cancer Center, University of Texas, Houston, Texas,4 AIDS Vaccine Program, SAIC/Frederick, Inc., National Cancer Institute, Frederick, Maryland5

Received 13 November 2003/ Accepted 21 January 2004

In this study, we analyzed the phenotypic and physiological consequences of the interaction of plasmacytoid dendritic cells (pDCs) with human immunodeficiency virus type 1 (HIV-1). pDCs are one cellular target of HIV-1 and respond to the virus by producing alpha/beta interferon (IFN-{alpha}/ß) and chemokines. The outcome of this interaction, notably on the function of bystander myeloid DC (CD11c+ DCs), remains unclear. We therefore evaluated the effects of HIV-1 exposure on these two DC subsets under various conditions. Blood-purified pDCs and CD11c+ DCs were exposed in vitro to HIV-1, after which maturation markers, cytokine production, migratory capacity, and CD4 T-cell stimulatory capacity were analyzed. pDCs exposed to different strains of infectious or even chemically inactivated, nonreplicating HIV-1 strongly upregulated the expression of maturation markers, such as CD83 and functional CCR7, analogous to exposure to R-848, a synthetic agonist of toll-like receptor-7 and -8. In addition, HIV-1-activated pDCs produced cytokines (IFN-{alpha} and tumor necrosis factor alpha), migrated in response to CCL19 and, in coculture, matured CD11c+ DCs, which are not directly activated by HIV. pDCs also acquired the ability to stimulate naïve CD4+ T cells, albeit less efficiently than CD11c+ DCs. This HIV-1-induced maturation of both DC subsets may explain their disappearance from the blood of patients with high viral loads and may have important consequences on HIV-1 cellular transmission and HIV-1-specific T-cell responses.

* Corresponding author. Mailing address: The NYU School of Medicine, Departments of Pathology and Medicine, MSB507, 550 First Ave., New York, NY 10016. Phone: (212) 263-5814. Fax: (212) 263-6729. E-mail: bhardn02{at}med.nyu.edu.

{dagger} J.-F.F. and M.L. contributed equally to this work.

Journal of Virology, May 2004, p. 5223-5232, Vol. 78, No. 10
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.10.5223-5232.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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