Molecular Profiling of Frontal Fibrosing Alopecia Reveals TH1 and JAK-STAT Up-Regulation with No Suppression of Hair Keratins

    April 2018 in “ Journal of Investigative Dermatology ”
    Jesús Gay-Mimbrera, Juan Ruano, Ana B. Pavel, R.D. Sanyal, N. Zhang, Yeriel Estrada, Emma Guttman‐Yassky
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    TLDR Frontal fibrosing alopecia shows increased inflammation and JAK-STAT pathway activity without reduced hair proteins.
    The document presents findings from a study on the molecular profile of frontal fibrosing alopecia (FFA), which included 12 patients with FFA, 10 with alopecia areata (AA), and 3 healthy controls. The study revealed that FFA tissues had higher levels of TH1 (IFN-γ, CXCL9, CXCL10) and JAK-STAT signaling mediators (JAK3, STAT1, IL-2RA), as well as several TH2/TH9 markers (IL-10, CCL13, IL-13, IL-9), even in non-lesional scalp compared to controls and AA tissues. The TH17/T22-regulated marker S100A7 was also upregulated in FFA lesions and correlated with clinical severity. Unlike AA, hair keratins were not suppressed in FFA. This research suggests that FFA is a highly inflammatory disease with predominant TH1 and JAK-STAT pathway involvement, identifying JAK-STAT signaling as a potential therapeutic target for FFA.
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