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已发表论文
朗格汉斯细胞在皮肤纤维化中的作用：转化生长因子-β1 信号轴
Authors Lv X, Xiang C, Zheng Y, Lv XL , Zhou WX
Received 25 June 2025
Accepted for publication 11 October 2025
Published 27 October 2025 Volume 2025:18 Pages 2801—2828
DOI https://doi.org/10.2147/CCID.S549199
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Jeffrey Weinberg
Xiong Lv, Chun Xiang, Yan Zheng, Xu-Ling Lv, Wan-Xuan Zhou
Department of Plastic Surgery, Quzhou People’s Hospital (Quzhou Affiliated Hospital of Wenzhou Medical University), Quzhou, Zhejiang, People’s Republic of China
Correspondence: Wan-Xuan Zhou, Email zhouzwx29@163.com
Abstract: Cutaneous fibrosis – including hypertrophic scars and keloids – arises when immune, epithelial, and stromal signals fail to re-equilibrate after injury. Langerin+ dendritic cells (DCs) – epidermal Langerhans cells and dermal cDC1 – sit at the center of this process. These DC subsets generate latent transforming growth factor-β 1 (TGF-β 1) that keratinocyte integrins αvβ 6/αvβ 8 locally activate, creating an epidermal “cytokine gate” that restrains immunity in homeostasis yet seeds fibrosis when overdriven. Downstream, active TGF-β 1 cooperates with mechanosensitive YAP/TAZ to drive fibroblast activation and matrix stiffening, while immune skewing (Th2/Th17/Treg and M2 macrophages) sustains a pro-fibrotic milieu. We synthesize how epithelial integrins, DC programs, and fibroblast mechanotransduction converge on TGF-β 1; compare normal wound resolution with hypertrophic scar and keloid; highlight insights from single-cell and spatial omics; and outline therapeutic strategies targeting the αv integrin–TGF-β 1 axis, YAP/TAZ, and immune cues. Framing cutaneous fibrosis through a DC-centric lens clarifies testable hypotheses and points toward mechanism-guided, combinatorial therapies.
Keywords: cutaneous fibrosis, Langerin+ dendritic cells, TGF-β 1 activation, hypertrophic scar, keloid, extracellular matrix remodeling
Department of Plastic Surgery, Quzhou People’s Hospital (Quzhou Affiliated Hospital of Wenzhou Medical University), Quzhou, Zhejiang, People’s Republic of China
Correspondence: Wan-Xuan Zhou, Email zhouzwx29@163.com
Abstract: Cutaneous fibrosis – including hypertrophic scars and keloids – arises when immune, epithelial, and stromal signals fail to re-equilibrate after injury. Langerin+ dendritic cells (DCs) – epidermal Langerhans cells and dermal cDC1 – sit at the center of this process. These DC subsets generate latent transforming growth factor-β 1 (TGF-β 1) that keratinocyte integrins αvβ 6/αvβ 8 locally activate, creating an epidermal “cytokine gate” that restrains immunity in homeostasis yet seeds fibrosis when overdriven. Downstream, active TGF-β 1 cooperates with mechanosensitive YAP/TAZ to drive fibroblast activation and matrix stiffening, while immune skewing (Th2/Th17/Treg and M2 macrophages) sustains a pro-fibrotic milieu. We synthesize how epithelial integrins, DC programs, and fibroblast mechanotransduction converge on TGF-β 1; compare normal wound resolution with hypertrophic scar and keloid; highlight insights from single-cell and spatial omics; and outline therapeutic strategies targeting the αv integrin–TGF-β 1 axis, YAP/TAZ, and immune cues. Framing cutaneous fibrosis through a DC-centric lens clarifies testable hypotheses and points toward mechanism-guided, combinatorial therapies.
Keywords: cutaneous fibrosis, Langerin+ dendritic cells, TGF-β 1 activation, hypertrophic scar, keloid, extracellular matrix remodeling