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Dendritic epidermal T cells facilitate wound healing in diabetic mice. 2016

Zhongyang Liu, and Yingbin Xu, and Lei Chen, and Julin Xie, and Jinming Tang, and Jingling Zhao, and Bin Shu, and Shaohai Qi, and Jian Chen, and Guangping Liang, and Gaoxing Luo, and Jun Wu, and Weifeng He, and Xusheng Liu
Department of Burns, The First Affiliated Hospital of Sun Yat-sen University Guangzhou, 510080, Guangdong, 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.

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