Dendritic cells (DCs) throughout the female reproductive tract (FRT) were examined for phenotype, HIV capture ability and innate anti-HIV responses. Two main CD11c + DC subsets were identified: CD11b + and CD11b low DCs. CD11b + CD14 + DCs were the most abundant throughout the tract. A majority of CD11c + CD14 + cells corresponded to CD1c + myeloid DCs, whereas the rest lacked CD1c and CD163 expression (macrophage marker) and may represent monocyte-derived cells. In addition, we identified CD103 + DCs, located exclusively in the endometrium, whereas DC-SIGN + DCs were broadly distributed throughout the FRT. Following exposure to GFP-labeled HIV particles, CD14 + DC-SIGN + as well as CD14 + DC-SIGN-cells captured virus, with ∼30% of these cells representing CD1c + myeloid DCs. CD103 + DCs lacked HIV capture ability. Exposure of FRT DCs to HIV induced secretion of CCL2, CCR5 ligands, interleukin (IL)-8, elafin, and secretory leukocyte peptidase inhibitor (SLPI) within 3 h of exposure, whereas classical pro-inflammatory molecules did not change and interferon-2 and IL-10 were undetectable. Furthermore, elafin and SLPI upregulation, but not CCL5, were suppressed by estradiol pre-Treatment. Our results suggest that specific DC subsets in the FRT have the potential for capture and dissemination of HIV, exert antiviral responses and likely contribute to the recruitment of HIV-Target cells through the secretion of innate immune molecules.