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
TLDR Targeting specific cell interactions may help treat skin fibrosis.
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.
