ACKR2 Limits Skin Fibrosis and Hair Loss Through IFN-β

The study investigated the role of the atypical chemokine receptor ACKR2 in skin fibrosis and hair loss, focusing on its interaction with the cytokine IFN-β. Researchers found that mice lacking ACKR2 (ACKR2−/−) exhibited increased skin fibrosis, characterized by thickening of the epidermis and dermis, loss of subcutaneous fat, disorganized collagen, and hair follicle deformation compared to wild-type mice. These mice also showed lower levels of pro-resolving mediators like IFN-β and IL-10, and higher levels of pro-inflammatory and pro-fibrotic cytokines. Treatment with exogenous IFN-β partially reversed these fibrotic changes and reduced lesion size, suggesting that ACKR2 limits skin fibrosis and hair loss by promoting IFN-β production, which aids in resolving inflammation and minimizing tissue scarring.