Type 17 immune responses are primarily mediated by Th17 cells and their effector cytokine interleukin-17 (IL-17), exerting a dual influence on wound healing. IL-17 plays a protective role during the initial stages of acute injury by facilitating rapid neutrophil recruitment, inducing antimicrobial peptide production and reinforcing pro-inflammatory signaling. However, sustained high signal of IL-17 results in a persistent inflammatory response that impairs keratinocyte proliferation and migration, angiogenesis, and nerve regeneration. This review elucidates the IL-17 signal effects and Th17 subset plasticity, which determines wound healing and skin barrier repair through their interactions with microbiota–immune, neuro–immune and metabolic reprogramming systems. Finally, we propose that the new therapeutic methods focus on IL-17 targets through precise spatiotemporal modulation and microenvironmental remodeling to create effective treatments for chronic non-healing wounds.
Lu et al. (Wed,) studied this question.