The skin is our largest organ and a natural barrier against frequent insults such as physical injury. Wound induced breaches to this barrier need to be restored as quickly as possible. Inability to properly repair skin integrity poses a great risk for infections and strongly impacts the quality of life. A crucial step in wound healing is the removal of apoptotic cells present at the injury site, typically performed by phagocytes as part of an anti-inflammatory process called efferocytosis. We have recently shown that inhibiting the cystine-glutamate antiporter SLC7A11 enhances efferocytosis by dendritic cells (DCs) and accelerates wound closure in mice. However, how this inhibition affects dermal DCs at a transcriptional and functional level (dealing with a high corpse burden, migration to the draining lymph nodes, antigen presentation, and T cell activation) and how DC-mediated efferocytosis ultimately impacts tissue repair during the different phases of wound healing is unknown. Using a combination of transgenic mice, in vivo efferocytosis and immunological assays and single-cell transcriptomic analyses of wounded skin, I aim to unravel how efferocytosis by dermal DCs contributes to cutaneous wound healing.