Dendritic cells (DCs) are antigen presenting cells with capacity to initiate primary T cell responses against pathogens such as HIV-1. In addition, DCs express receptors required for HIV-1 infection and are probably one of the first target cells during mucosal transmission of HIV-1. Their localization in mucosal epithelial and in the T cell areas of lymphoid organs as well as their role in capturing antigen and initiating T cell responses, highlights their importance during HIV-1 pathogenesis. We have studied the effects of HIV-1 infection on DC function. We found that monocyte-derived DCs were productively infected by HIV-1 after in vitro exposure. HIV1 infected monocyte-derived DCs upregulated co-stimulatory molecules in response to CD40L stimulation comparable to uninfected DCs. However, intracellular cytokine staining revealed that HIV-1 infected DCs failed to produce IL12p70, although they could respond with TNF-alpha production. This may impact the ability of DCs to induce optimal HIV-1 specific immune responses. In addition, we found a differential susceptibility to HIV-1 infection of primary isolated myeloid and plasmacytoid dendritic cells. Productively infected myeloid and plasmacytoid DCs efficiently transferred HIV-1 to autolgous CD4+ T cells and antigen-reactivated T cells were more frequently infected than resting T cells. Altogether, these findings suggest that DCs are under certain conditions impaired by HIV-1 infection but can still transfer HIV-1 to CD4+ T cells.
