ArticleEMBO molecular medicine2024
JAK-STAT1 as therapeutic target for EGFR deficiency-associated inflammation and scarring alopecia.
Article in EMBO molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Vitamin E promotes dermal papilla cell proliferation via the lncRNA2919/STAT1 axis to activate the Hedgehog signaling pathway.Non-coding RNA research · 2026Article
- Down-regulation of Shh in the hair follicles of mice during chemotherapy-induced hair loss is mediated by the JAK/STAT1 signaling pathway.FEBS open bio · 2026Article
- Disruption of metabolic licensing by JAK inhibitors constrains CD8 T cell activation and effector function.Cell death & disease · 2026Article
- Prevention and Management of Dermatologic Adverse Events in Patients Treated with Amivantamab Plus Lazertinib.Current oncology (Toronto, Ont.) · 2026Article
- Chinese botanical drugs for mitigating epidermal growth factor receptor-targeted therapy-associated cutaneous toxicity: immune mechanisms and translational pathways.Frontiers in pharmacology · 2026Review
- Papulopustular eruptions associated with EGFR-pathway-related targeted therapies: clinical spectrum, evidence boundaries, folliculocentric inflammation, and management considerations.Frontiers in oncology · 2026Review
- Recent Advances in the Role of Fibroblast Growth Factors in Hair Follicle Growth.Biomolecules · 2025Review
- EGFR controls transcriptional and metabolic rewiring in KRASEMBO molecular medicine · 2025Article
- Review
- Integrative systems biology framework discovers common gene regulatory signatures in mechanistically distinct inflammatory skin diseases.NPJ systems biology and applications · 2025Article
- Vitamin K supports TGF-β1 dependedFrontiers in immunology · 2025Article
- Case Report: A novel KRT74 variant in an eight-year-old boy with alopecia totalis successfully treated with baricitinib.Frontiers in medicine · 2025Article
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
The hair follicle stem cell niche is an immune-privileged microenvironment, characterized by reduced antigen presentation, thus shielding against permanent immune-mediated tissue damage. In this study, we demonstrated the protective role of hair follicle-specific epidermal growth factor receptor (EGFR) against scarring hair follicle destruction. Mechanistically, disruption of EGFR signaling generated a cell-intrinsic hypersensitivity within the JAK-STAT1 pathway, which, synergistically with interferon gamma expressing CD8 T-cell and NK-cell-mediated inflammation, compromised the stem cell niche. Hair follicle-specific genetic depletion of either JAK1/2 or STAT1 or therapeutic inhibition of JAK1/2 ameliorated the inflammation, restored skin barrier function and activated the residual stem cells to resume hair growth in mouse models of epidermal and hair follicle-specific EGFR deletion. Skin biopsies from EGFR inhibitor-treated and cicatricial alopecia patients revealed an active JAK-STAT1 signaling signature along with upregulation of antigen presentation and downregulation of key components of the EGFR pathway. Our findings offer molecular insights and highlight a mechanism-based therapeutic strategy for addressing chronic folliculitis associated with EGFR-inhibitor anti-cancer therapy and cicatricial alopecia.
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