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Comment
. 2022 Oct 8;7(1):359.
doi: 10.1038/s41392-022-01202-9.

IL-17 signaling in skin repair: safeguarding metabolic adaptation of wound epithelial cells

Juan Wang  1   2 , Xiaolei Ding  3   4
Affiliations
Comment

IL-17 signaling in skin repair: safeguarding metabolic adaptation of wound epithelial cells

Juan Wang et al. Signal Transduct Target Ther. .
No abstract available

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Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
IL-17A signaling promotes epithelization by shaping wound epithelial cell metabolism. (Top) The scheme illustrates cellular networks involved in wound healing progression. Upon injury, immune cells, including neutrophils, macrophages, and lymphocytes, initiate an inflammatory response, which orchestrates wound healing progression. Fibroblasts become myofibroblasts, contributing to granulation formation. The activated keratinocytes at the wound edge migrate over the freshly formed granulation, re-epithelizing and restoring skin barrier function. Konieczny and colleagues report that RORγt + γδ T-cell-derived IL-17A regulates wound epithelization. (Bottom) RORγt + γδ T-cell-derived IL-17A signaling is required for the glycolytic metabolism and migration of wound epithelial tongue cells. IL-17A binds to its receptor IL-17-RC and induces HIF1α expression through ERK/AKT activated mTOR signaling. IL-17A-HIF1α signaling axis-mediated glycolytic metabolism is essential for the migratory activity of wound keratinocytes, thereby regulating wound epithelization
See this image and copyright information in PMC

Comment on

  • Interleukin-17 governs hypoxic adaptation of injured epithelium.
    Konieczny P, Xing Y, Sidhu I, Subudhi I, Mansfield KP, Hsieh B, Biancur DE, Larsen SB, Cammer M, Li D, Landén NX, Loomis C, Heguy A, Tikhonova AN, Tsirigos A, Naik S. Konieczny P, et al. Science. 2022 Jul 8;377(6602):eabg9302. doi: 10.1126/science.abg9302. Epub 2022 Jul 8. Science. 2022. PMID: 35709248 Free PMC article.

References

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