HSV initially infects the stratified squamous epithelium of skin and anogenital mucosa, prior to entering nerve endings and establishing lifelong latent infection. We previously reported that topical application of HSV-1 to human inner foreskin explants, simulating in vivo infection, resulted in infection of epidermal Langerhans cells (LCs), which then emigrated into the dermis and clustered with dermal dendritic cells (dDCs). The HSV-infected LCs also underwent apoptosis and were taken up by subsets of dDCs (1). To define the mechanism of these interactions, we sought to determine the “find me” and “eat me” signals that attract human dDCs to HSV-infected LCs, and facilitate recognition and uptake of apoptotic LCs. Using RNA-seq, flow cytometry and ELISA, we assessed the expression of chemokines in HSV-infected LCs and corresponding chemokine receptors on the dDC subsets, as well as apoptotic receptors that may recognise and facilitate their interactions. Differential expression of several chemokine receptors was observed, including CCR5 on CD14⁺DCs and CXCR3 on cDC1s (CD141/XCR1⁺). The CXCR3 ligand CXCL10 was observed in HSV-infected LCs by RNA-seq and ELISA. Several apoptotic receptors have been observed on dDCs including TAM family receptors Tyro3 and Mer, ICAM3, CD36, MFG-E8 and Integrin αVβ3. The relative importance of these chemokine-receptor pairs and apoptotic receptors are being established for each dDC subset. In biopsies of initial genital herpes lesions, in the superficial dermis interfacing with the dermo-epidermal junction, infiltrating CD4⁺ and CD8⁺T cells were observed. The dDC subsets also had differing spatial distributions in the superficial and deep dermis, and there was selective contact of CD8⁺T cells with the cDC1s. These studies defining the mechanisms of uptake and viral antigen transfer between LCs and dDCs, leading to subsequent presentation to CD4⁺ and CD8⁺T cells may define potential DC targets for adjuvants in future mucosal or intradermal vaccines.