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Am J Transl Res. 2016 May 15;8(5):2375-84. eCollection 2016.

Dendritic epidermal T cells facilitate wound healing in diabetic mice.

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Department of Burns, The First Affiliated Hospital of Sun Yat-sen University Guangzhou, 510080, Guangdong, P. R. China.
State Key Laboratory of Trauma, Burn and Combined Injury, Institute of Burn Research, Southwest Hospital, The Third Military Medical UniversityChongqing 400038, P. R. China; Chongqing Key Laboratory for Disease ProteomicsChongqing 400038, P. R. China.


The impairment of skin repair in diabetic patients can lead to increased morbidity and mortality. Proper proliferation, apoptosis and migration in keratinocytes are vital for skin repair, but in diabetic patients, hyperglycemia impairs this process. Dendritic epidermal T cells (DETCs) are an important part of the resident cutaneous immunosurveillance program. We observed a reduction in the number of DETCs in a streptozotocin-induced diabetic mouse model. This reduction in DETCs resulted in decreased IGF-1 and KGF production in the epidermis, which is closely associated with diabetic delayed wound closure. DETCs ameliorated the poor wound-healing conditions in diabetic mice by increasing keratinocyte migration and proliferation and decreasing keratinocyte apoptosis in diabetes-like microenvironments. Our results elucidate a new mechanism for diabetic delayed wound closure and point to a new strategy for the treatment of wounds in diabetic patients.


Diabetes; dendritic epidermal T cells; wound healing


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