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Prepublished online as a Blood First Edition Paper on February 6, 2003; DOI 10.1182/blood-2002-10-3189. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-10-3189v1 101/11/4505    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Donaghy, H. Articles by Patterson, S. Search for Related Content PubMed PubMed Citation Articles by Donaghy, H. Articles by Patterson, S. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 June 2003, Vol. 101, No. 11, pp. 4505-4511 IMMUNOBIOLOGY Dysfunction and infection of freshly isolated blood myeloid and plasmacytoid dendritic cells in patients infected with HIV-1 Heather Donaghy, Brian Gazzard, Frances Gotch, and Steven Patterson From the Department of Immunology, Imperial College of Science, Technology and Medicine, Chelsea and Westminster Hospital, London, United Kingdom; and the Department of HIV/GU Medicine, Chelsea and Westminster Hospital, London, United Kingdom. Recently it has been shown that the 2 populations of blood dendritic cells (DCs), termed plasmacytoid (pcDCs) and myeloid (myDCs), are reduced in HIV-1 infection. This study aimed to determine whether these 2 populations are targets for HIV-1 infection and whether their ability to stimulate T-lymphocyte proliferation is affected. Highly purified populations of myDCs and pcDCs were isolated from the blood of antiretroviral treatment–naive patients and assessed for the level of HIV provirus by polymerase chain reaction (PCR). We show that both populations are targets for HIV-1 infection as indicated by the presence of provirus in 12 of 14 pcDC and 13 of 14 myDC samples tested. A proportion of this provirus is integrated in myDCs. The ability of both myDCs and pcDCs from HIV-1–infected patients to stimulate allogeneic T-lymphocyte proliferation in a 6-day mixed leukocyte reaction was severely impaired, but was not mediated by secondary infection of T lymphocytes. Thus, in addition to depletion, both myeloid and plasmacytoid DCs are infected and show impaired functional capacity. These findings suggest that infection, depletion, and dysfunction of dendritic cells may contribute to the immunosuppression associated with HIV-1 disease. 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