The Double-Edged Sword of Type 17 Immunity in Wound Healing and Skin Barrier Repair: Microenvironment-Driven Functional Plasticity

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

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.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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