Connection between T regulatory cell enrichment and collagen deposition in keloid.

Keloid is a dermal tumor with high recurrence rate. The immune system plays a critical role in preventing pathogen infiltration, inducing inflammation, initiating downstream processes, and recruiting fibrocytes in keloids. Interestingly, we observed a local, but not systemic, enrichment of Treg cells and Treg-associated gene expression at the keloid lesions compared to non-keloid tissues. Concurrently, keloid tissues presented significantly elevated expression of type I and type III collagen. Moreover, the level of collagen III and the collagen III-to-collagen I ratio were positively correlated with the level of FOXP3. To investigate whether Treg cells could directly promote the expression of collagen, fibrocytes were cocultured with autologous Treg cells. Activated Treg cells, but not quiescent Treg cells, were capable of promoting collagen expression. This response was more pronounced in keloid patients than in non-keloid controls, and required the secretion of TGF-ß. Overall, these findings demonstrated a connection between collagen overexpression and imbalance and Treg dysregulation in keloid tissues.