Scarring Alopecia Is Driven by the Collapse of EGFR-Protected JAK-STAT1-Sensitive Stem Cell Immune Privilege

    Karin Strobl, Jörg Klufa, R. Jin, L. Artner-Gent, Dana Krauß, P. Novoszel, Johanna Strobl, Georg Stary, Igor Vujic, J. Griss, Martin Holcmann, M. Farlik, Bernhard Homey, Maria Sibilia, Thomas Bauer
    TLDR Cancer treatment drugs can cause permanent hair loss by damaging hair follicle stem cells, but a specific inhibitor might reverse this effect.
    Long-term treatment with EGFR inhibitors can lead to inflammatory scarring alopecia by causing hyper-activation of JAK-STAT1 signaling, which collapses the immune privilege of hair follicle stem cells. A mouse model with hair follicle-specific deletion of EGFR showed that therapeutic inhibition of JAK1/2 can restore immune privilege and stimulate hair growth. Translational studies confirmed STAT1 pathway activation in patients treated with EGFR inhibitors and those with certain types of alopecia. A case study demonstrated successful treatment of folliculitis decalvans with the JAK1/2 inhibitor Baricitinib, suggesting potential therapeutic strategies for scarring alopecia linked to EGFR-inhibitor therapy.
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