促炎细胞因子
伤口愈合
FOXP3型
炎症
免疫学
巨噬细胞
癌症研究
伤口闭合
生物
细胞生物学
医学
免疫系统
体外
生物化学
作者
Audrey Nosbaum,Nicolas Prevel,Hong-An Truong,Pooja Mehta,Monika Ettinger,Tiffany C. Scharschmidt,Niwa Ali,Mariela Pauli,Abul K. Abbas,Michael D. Rosenblum
出处
期刊:Journal of Immunology
[American Association of Immunologists]
日期:2016-01-30
卷期号:196 (5): 2010-2014
被引量:405
标识
DOI:10.4049/jimmunol.1502139
摘要
Foxp3-expressing regulatory T cells (Tregs) reside in tissues where they control inflammation and mediate tissue-specific functions. The skin of mice and humans contain a large number of Tregs; however, the mechanisms of how these cells function in skin remain largely unknown. In this article, we show that Tregs facilitate cutaneous wound healing. Highly activated Tregs accumulated in skin early after wounding, and specific ablation of these cells resulted in delayed wound re-epithelialization and kinetics of wound closure. Tregs in wounded skin attenuated IFN-γ production and proinflammatory macrophage accumulation. Upon wounding, Tregs induce expression of the epidermal growth factor receptor (EGFR). Lineage-specific deletion of EGFR in Tregs resulted in reduced Treg accumulation and activation in wounded skin, delayed wound closure, and increased proinflammatory macrophage accumulation. Taken together, our results reveal a novel role for Tregs in facilitating skin wound repair and suggest that they use the EGFR pathway to mediate these effects.
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