CD4+CD8+ double-positive mature peripheral T-cells (DPs) are detectable in a variety of tissues. However, despite their relevant implications in autoimmune and malignant skin disorders, such as atopic dermatitis and cutaneous T-cell lymphoma, very little is known about their role or function; likely due to their very low abundance. Additionally, technical difficulties that confound distinguishing DP single-cells from CD4+-CD8+ T-cell aggregates makes them difficult to study. We have overcome these issues using a novel isolation strategy which allows us to obtain >95% pure DPs. To determine whether peripheral DPs arise from CD4+ T-cells, we adoptively transferred highly purified single-positive T-cells into Rag1-/- mice. Under these conditions we observed that subsets of CD4+ T-cells become DP T-cells with the peculiarity that these cells express CD8a but not CD8b, which is in contrast to DPs isolated from wild-type mice. To study the effect of DPs on the regulation of skin CD8+ T-cells, we used a contact hypersensitivity model (CHS). Recipient animals were sensitized with Ovalbumin (OVA) in the flank a week prior to the injection of pure naïve DPs or OVA-immunized DPs. One day after T cell infusion, ears were challenged with an intradermal injection of OVA and thickness of the ears was measured as an indicator of CD8 T cell-induced inflammation. As expected, OVA-challenged ears from animals which received no cells showed a 40% increase in ear thickness compared with PBS-challenged control ears. Interestingly, the transfer of a low number of DPs significantly suppressed CD8+ T-cell dependent inflammation. Moreover, the DP inhibitory phenotype depended on their activation status since only activated and not naïve DPs prevented skin inflammation. Our data suggests a powerful immunoregulatory role for DPs in controlling CD8+ T-cell function in the skin.