Dendritic cells (DC) from human peripheral blood are susceptible to productive and probably to latent infection with HIV-I [18, 29]. Infection of DC also occursin vivosince in HIV-seropositive individuals Langerhans’cells of the skin [16] and DC from peripheral blood ([17], in preparation) are infected. In peripheral blood 3–25% of DC, identified as large, low-density cells lacking monocyte markers, are infected as judged byin situhybridization with an HIV probe. This contrasts with the lower proportion (<0.2%) of other cells infected. DC exposed to HIVin vitroorin vivofail to present other antigens or mitogens to stimulate T cells [29, 38, 41]. This functional defect in infected DC is not blocked by the presence of soluble CD4 antigen and occurs in the absence of T cell infection suggesting a block at the level of the antigen-presenting cell itself. Infection, depletion and dysfunction of DC in HIV seropositive patients is already present in asymptomatic individuals and this precedes the appearance of T cell defects. We speculate that loss of functional DC may be a fundamental defect leading to a block in recruitment of resting T cells into immune responses.In contrast to the HIV-induced impairment of antigen presentation by DC, these cells were potent stimulators of responses to the HIV antigens themselves. Normal DC infected with HIVin vitrostimulated primary proliferative and cytotoxic T cell responses ([52], in preparation). These were produced in cells from individuals expressing a range of different MHC types but the cytotoxic cells, once produced, killed autologous but not allogeneic, infected T cell blasts. Primary response to viral peptides can also be produced suggesting that this system may be useful for identifying immunogenic epitopes of HIV using cells from sero-negative, non-immunocompromised individuals.