Frontal Fibrosing Alopecia Shows Robust T Helper 1 and Janus Kinase 3 Skewing

June 2020 in “ British journal of dermatology/British journal of dermatology, Supplement ”

Ester Del Duca, Juan Ruano, Ana B. Pavel, R.D. Sanyal, Teresa Song, Jesús Gay-Mimbrera, N. Zhang, Yeriel Estrada, Xiangyu Peng, Yael Renert‐Yuval, Robert Phelps, Ralf Paus, James G. Krueger, Emma Guttman‐Yassky

TLDR Frontal fibrosing alopecia is linked to increased immune system activity and reduced stem cells, suggesting early treatment targeting this pathway might prevent hair follicle damage.

The study investigated the pathogenesis of Frontal fibrosing alopecia (FFA) by comparing scalp biopsies from 12 FFA patients, 8 alopecia areata (AA) patients, and 8 controls, focusing on gene and protein expression. The results showed significant increases in CD8+ cytotoxic T cells, CD11c+ dendritic cells, and tissue-resident memory T cells in FFA and AA compared to controls, with a notable upregulation of granzyme B mRNA in FFA. FFA was characterized by a significant upregulation of T helper 1/interferon (IFN) and the Janus kinase/signal transducers and activators of transcription (JAK-STAT) pathway, as well as fibrosis-related products, without the downregulation of hair keratins and T-regulatory markers seen in AA. Additionally, stem cell markers were significantly reduced in FFA. These findings suggest that immune-mediated attack in the bulge region of the hair follicle, followed by fibrosis and a decrease in stem cells, may contribute to follicular damage in FFA. The study implies that JAK/STAT-targeting treatments could potentially prevent permanent follicular destruction and fibrosis if applied in the early stages of the disease.

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