Dendritic cells at the interface of innate and adaptive immunity to HIV-1Smed-Sörensen, Annaa; Loré, KarinbCurrent Opinion in HIV & AIDS: September 2011 - Volume 6 - Issue 5 - p 405–410 doi: 10.1097/COH.0b013e328349b06b Innate immunity: Edited by William A. Paxton and Teunis B.H. Geijtenbeek Abstract Author Information Purpose of review: This review summarizes recent findings on how HIV-1 infection affects dendritic cells in their ability to elicit innate and adaptive immune responses. Recent findings: The phenomenon describing a reduction of dendritic cell numbers in the blood of HIV-1-infected individuals has been expanded on in recent studies demonstrating that dendritic cells decline very early in primary infection and that there is a mobilization of semi-mature dendritic cells to lymph nodes. Recent data suggest that dendritic cells in lymph nodes are more prone to apoptosis, which correlates with disease progression. In addition, plasmacytoid dendritic cells isolated from blood showed a semi-mature phenotype after HIV-1 exposure, which coincided with persistent IFN-α secretion. Emerging data show that semi-mature dendritic cells induce regulatory T cells and suppress effector function. There may therefore be mechanisms by which HIV-1 affects dendritic cell immune stimulation and, in doing so, interferes with the elicitation of anti-HIV-1 responses. Summary: Understanding how dendritic cells are functionally altered during HIV-1 infection is crucial for the development of new immune-therapy strategies including approaches to target dendritic cells with antigen in vivo or ex vivo to induce efficient adaptive anti-HIV immunity. aDepartment of Microbiology, Tumor and Cell Biology bCenter for Infectious Medicine, Department of Medicine, Karolinska Institutet, Stockholm, Sweden Correspondence to Dr Anna Smed-Sörensen, Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, 171 77 Stockholm, SwedenTel: +46 8 524 86952; e-mail: firstname.lastname@example.org © 2011 Lippincott Williams & Wilkins, Inc.