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

    November 2024 in “ EMBO Molecular Medicine ”
    Karoline Strobl, Jörg Klufa, Regina Jin, Lena Artner-Gent, Dana Krauß, Philipp Novoszel, Johanna Strobl, Georg Stary, Igor Vujic, Johannes Griss, Martin Holcmann, Matthias Farlik, Bernhard Homey, Maria Sibilia, Thomas Bauer
    TLDR Targeting JAK-STAT1 can reduce inflammation and promote hair growth in conditions linked to EGFR deficiency.
    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.
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