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Blood, 1 November 2004, Vol. 104, No. 9, pp. 2810-2817. Prepublished online as a Blood First Edition Paper on July 1, 2004; DOI 10.1182/blood-2003-07-2314. This Article Full Text (PDF) All Versions of this Article: 2003-07-2314v1 104/9/2810    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Smed-Sorensen, A. Articles by Spetz, A.-L. Search for Related Content PubMed PubMed Citation Articles by Smed-Sorensen, A. Articles by Spetz, A.-L. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted July 10, 2003 Accepted June 9, 2004 HIV-1 infected dendritic cells upregulate cell surface markers but fail to produce IL-12 p70 in response to CD40ligand stimulation Anna Smed-Sorensen*, Karin Lore, Lilian Walther-Jallow, Jan Andersson, and Anna-Lena Spetz Department of Medicine, Center for Infectious Medicine, Karolinska Institute, Karolinska University Hospital Huddinge, Stockholm, Sweden National Institutes of Health, Vaccine Research Center, Bethesda, Maryland, USA * Corresponding author; email: anna.smed.sorensen{at}medhs.ki.se. Dendritic cells (DCs) are antigen-presenting cells with the capacity to prime naive T cells for efficient cellular responses against pathogens such as HIV-1. DCs are also susceptible to HIV-1 infection, which may impair their ability to induce immunity. Here, we examined the ability of HIV-1 infected in vitro-derived DCs to respond to CD40ligand (CD40L) stimulation with the aim to study events during early HIV-1 infection. HIV-1BaL infected p24+ DCs were detected after only 3 days of exposure to highly concentrated virus. We show that HIV-1 infected DCs upregulated co-stimulatory molecules, but were skewed in their production of effector cytokines in response to CD40L stimulation. CD40L stimulation induced significant secretion of TNF and IL-12 p70 from both HIV-1 exposed and unexposed DCs. Intracellular stainings of HIV-1 exposed DCs revealed that TNF could be detected in both the p24- and p24+ DCs, but IL-12 p70 could only be found in the p24- DCs. Thus, while p24+ DCs showed a similar mature phenotype as p24- DCs after CD40L stimulation, they appeared to have an impaired cytokine profile. 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