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
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    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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