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

## TL;DR

This paper explores how Type 17 immunity, led by Th17 cells and IL-17, can both help and hinder wound healing and skin repair depending on the environment.

## Contribution

The paper introduces new therapeutic strategies targeting IL-17 with spatiotemporal precision and microenvironmental adjustments.

## Key findings

- IL-17 aids early wound healing by promoting neutrophil recruitment and antimicrobial activity.
- Prolonged IL-17 signaling causes chronic inflammation and delays healing by impairing keratinocyte and nerve functions.
- Therapeutic modulation of IL-17 and microenvironmental factors may improve outcomes in chronic wounds.

## Abstract

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.