Ultraviolet radiation-induced immunosuppression creates a permissive environment for skin tumour growth. We aimed to identify specific myeloid cell populations required for the modulation of UVR-mediated immunosuppression. Clodronate depletion during a burning dose of UV radiation as a neonate could prevent long-term immunosuppression measured with delayed-type contact hypersensitivity. Regulatory CD4+ T-cells are responsible for immune suppression and are not recruited to the same extent when neonates are clodronate depleted during UVR exposure. We believe the interaction between myeloid cells and immunosuppression is based on the reduced number of skin-resident CCR2-CD64+ macrophages, and altered recruitment of CCR2+Ly6c+MHCII+ dendritic cells caused by UVR. This data strongly shows the interplay between myeloid cells and T-cells involved in UVR-mediated immunosuppression and possible avenues for intervention.