Langerin+ Dendritic Cells In Cutaneous Fibrosis: The TGF-β1 Signaling Axis
October 2025
in “
Clinical Cosmetic and Investigational Dermatology
”
cutaneous fibrosis hypertrophic scars keloids Langerin+ dendritic cells TGF-β1 keratinocyte integrins cytokine gate YAP/TAZ fibroblast activation matrix stiffening αv integrin mechanotransduction skin fibrosis scar tissue immune cells transforming growth factor beta 1 skin cells cell signaling Yes-associated protein transcriptional coactivator with PDZ-binding motif cell activation tissue stiffening integrin cell mechanics
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.