Abstract
Whether resident and recruited myeloid cells may impair or aid healing of acute skin wounds remains a debated question. To begin to address this, we examined the importance of CD11c+ myeloid cells in the early activation of skin wound repair. We find that an absence of CD11c+ cells delays wound closure and epidermal proliferation, likely due to defects in the activation of the IL-23-IL-22 axis that is required for wound healing.
Highlights
To the Editor, Wound healing in healthy skin requires a complex interplay between immune and non-immune cells
To begin to address this, we examined the importance of CD11c+ myeloid cells in the early activation of skin wound repair
We find that an absence of CD11c+ cells delays wound closure and epidermal proliferation, likely due to defects in the activation of the IL-23-IL-22 axis that is required for wound healing
Summary
To the Editor, Wound healing in healthy skin requires a complex interplay between immune and non-immune cells. In addition to their roles in infection control and cell debridement, leukocytes secrete factors to orchestrate the timing of the repair process via crosstalk with epithelia. This critical role in wound timing is vital as failure to induce wound closure leads to debilitating chronic wounds susceptible to further infection and patient sepsis. We have shown that injury-induced activation of Notch signalling results in recruitment of type 3 innate lymphoid cells (ILC3s) that control macrophage recruitment and epidermal closure.[1] Injury initiates the rapid influx of innate myeloid cells to the skin; this influx is
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