BackgroundDiabetic ulcers (DUs) is a common complication of diabetes, for which the morbidity and mortality increasing annually worldwide. The deficiency of PD-L1 in keratinocytes (KCs) may be linked to the diabetic wound healing impediments. ObjectiveOur study utilized transgenic mice to assess the functions of epidermal KCs-specific PD-L1 in DUs treatment. Methods and resultsEpidermal KCs-specific PD-L1 knockouted mice demonstrate deteriorated healing rates, concomitant with exacerbated inflammatory infiltration and excessive angiogenesis. The streptozotocin-induced murine diabetes model was used to imitate DUs in-vivo context, and the delayed healing was found under diabetic conditions. We then generated transgenic mice overexpressing PD-L1 in the epidermis. PD-L1 overexpression accelerate the DUs healing process accompanied by a reduction in inflammatory infiltration and a corresponding decreasion of angiogenesis. Therefore, overexpression of PD-L1 accelerates the healing process of DUs. ConclusionIn sum, epidermal KCs-specific PD-L1 plays vital roles in epidermis regeneration, inflammatory infiltration, and angiogenesis during DUs restoration, and would not be easily to format fibrous scar. Our study elucidated a new therapeutic idea for slow-healing wound care.
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