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Langerin+ Dendritic Cells in Cutaneous Fibrosis: The TGF-β1 Signaling Axis.

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Titel: Langerin+ Dendritic Cells in Cutaneous Fibrosis: The TGF-β1 Signaling Axis.
Autoren: Lv, Xiong, Xiang, Chun, Zheng, Yan, Lv, Xu-Ling, Zhou, Wan-Xuan
Quelle: Clinical, Cosmetic & Investigational Dermatology; Oct2025, Vol. 18, p2801-2828, 28p
Schlagwörter: TRANSFORMING growth factors-beta, HYPERTROPHIC scars, THERAPEUTICS, LANGERHANS cells, KELOIDS, IMMUNE response, FIBROBLASTS
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. [ABSTRACT FROM AUTHOR]
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Datenbank: Biomedical Index
Beschreibung
Abstract:Cutaneous fibrosis – including hypertrophic scars and keloids – arises when immune, epithelial, and stromal signals fail to re-equilibrate after injury. Langerin<sup>+</sup> 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. [ABSTRACT FROM AUTHOR]
ISSN:11787015
DOI:10.2147/CCID.S549199