ACKR2 Limits Skin Fibrosis and Hair Loss Through IFN-β

The study demonstrated that the atypical chemokine receptor ACKR2 played a crucial role in limiting skin fibrosis and hair loss by modulating inflammation through IFN‐β. In ACKR2 −/− mice, there was increased skin thickening, collagen disorientation, and hair follicle loss compared to wild-type mice, alongside reduced levels of pro-resolving mediators like IFN‐β and IL‐10. Conversely, there were elevated levels of pro-inflammatory and pro-fibrotic cytokines. Treatment with exogenous IFN‐β partially reversed these fibrotic outcomes, suggesting that ACKR2, through IFN‐β, was vital in resolving inflammation and reducing tissue scarring.