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Background and Objectives <p>Keloids are problematic fibrotic lesions with excessive collagen and chronic inflammation; their underlying causes are not fully understood. Type 2 helper T (Th2) cytokines IL-4 and IL-13 are implicated in various fibrotic disorders, including but not limited to pulmonary fibrosis and systemic sclerosis. This study aimed to investigate the IL-4/IL-13 signaling pathway's contribution to keloid pathophysiology and evaluate its potential as a novel therapeutic target.</p> Methods <p>We retrospectively analyzed keloid patients, collecting demographic data and grading scar severity with the Vancouver Scar Scale (VSS). Keloid tissue specimens underwent immunofluorescence, Western blotting, and real-time PCR to quantify IL-4, IL-13, Type I Collagen alpha 1 (Collagen I A1), and phosphorylated STAT6 (p-STAT6) expression.</p> Results <p>Patients had an average total VSS score of 11.0 ± 2.9, indicating active fibrotic inflammation. Molecular assays showed significant upregulation of IL-4 and IL-13, alongside increased p-STAT6 and Collagen I A1 in keloid tissues. Notably, IL-4, IL-13, and p-STAT6 expression positively correlated with VSS thickness and pliability scores.</p> Conclusions <p>Our findings demonstrate that the IL-4/IL-13 signaling axis is markedly activated in keloid tissues, promoting collagen synthesis via STAT6 phosphorylation. Therefore, targeting the IL-4/IL-13/STAT6 pathway may represent a promising therapeutic strategy for managing keloids.</p>

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Exploration of novel therapeutic targets for keloids based on clinical and molecular data: the role of the IL-4/IL-13 signaling pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月17日

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  • Xueli Li,
  • Jianping Lan,
  • Ruoyun Liu,
  • Tingting Lin,
  • Zheqi Li,
  • Bo Cheng

摘要

Background and Objectives

Keloids are problematic fibrotic lesions with excessive collagen and chronic inflammation; their underlying causes are not fully understood. Type 2 helper T (Th2) cytokines IL-4 and IL-13 are implicated in various fibrotic disorders, including but not limited to pulmonary fibrosis and systemic sclerosis. This study aimed to investigate the IL-4/IL-13 signaling pathway's contribution to keloid pathophysiology and evaluate its potential as a novel therapeutic target.

Methods

We retrospectively analyzed keloid patients, collecting demographic data and grading scar severity with the Vancouver Scar Scale (VSS). Keloid tissue specimens underwent immunofluorescence, Western blotting, and real-time PCR to quantify IL-4, IL-13, Type I Collagen alpha 1 (Collagen I A1), and phosphorylated STAT6 (p-STAT6) expression.

Results

Patients had an average total VSS score of 11.0 ± 2.9, indicating active fibrotic inflammation. Molecular assays showed significant upregulation of IL-4 and IL-13, alongside increased p-STAT6 and Collagen I A1 in keloid tissues. Notably, IL-4, IL-13, and p-STAT6 expression positively correlated with VSS thickness and pliability scores.

Conclusions

Our findings demonstrate that the IL-4/IL-13 signaling axis is markedly activated in keloid tissues, promoting collagen synthesis via STAT6 phosphorylation. Therefore, targeting the IL-4/IL-13/STAT6 pathway may represent a promising therapeutic strategy for managing keloids.