JAK-STAT1 as Therapeutic Target for EGFR Deficiency-Associated Inflammation and Scarring Alopecia

The study explores the JAK-STAT1 pathway's role in scarring alopecia linked to EGFR deficiency, revealing that EGFR signaling disruption leads to JAK-STAT1 hypersensitivity and inflammation from CD8 T-cells and NK-cells, damaging hair follicle stem cells. In mouse models, genetic depletion or therapeutic inhibition of JAK1/2 reduces inflammation, restores skin function, and promotes hair regrowth. The research suggests JAK inhibitors as a promising treatment for scarring alopecia and adverse effects from EGFR-inhibitor cancer therapies. The study involved various analyses, including RNA sequencing and immunofluorescence, and used biopsy samples from 20 patients, highlighting the therapeutic potential of targeting the JAK-STAT1 pathway.