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

    Lv Xiong, Chun Xiang, Yan Zheng, Xu-Ling Lv, Wan-Xuan Zhou
    Cutaneous fibrosis, such as hypertrophic scars and keloids, occurs when immune, epithelial, and stromal signals fail to balance after injury. Langerin<sup>+</sup> dendritic cells (DCs) play a central role by producing latent TGF-β1, which is activated by keratinocyte integrins, forming a "cytokine gate" that can lead to fibrosis if overstimulated. Active TGF-β1, along with YAP/TAZ, promotes fibroblast activation and matrix stiffening, while immune responses maintain a pro-fibrotic environment. The study explores the interaction between epithelial integrins, DCs, and fibroblast mechanotransduction, comparing normal wound healing with fibrosis, and suggests therapeutic strategies targeting the αv integrin-TGF-β1 axis, YAP/TAZ, and immune signals. This DC-focused perspective offers new hypotheses and potential for mechanism-based therapies.
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