ArticleThe Journal of clinical investigation2020
Hair follicle stem cell replication stress drives IFI16/STING-dependent inflammation in hidradenitis suppurativa.
Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 49 citations in OpenAlex.
- Cross-species comparative spatial transcriptomics of hair follicle-T cell interactions identifies conserved drivers of cutaneous lupus erythematosus skin disease and associated hair loss.Nature communications · 2026Article
- Reducing Unmet Needs in Hidradenitis Suppurativa by Including the Hair Follicle Among an Arsenal of Targets.Experimental dermatology · 2026Review
- Single-cell spatial profiling identifies a mucosal-like epithelial signature in Hidradenitis suppurativa tunnels.JCI insight · 2026Article
- Hair follicle stem cell fate supports distinct clinical endotypes in hidradenitis suppurativa.Journal of the European Academy of Dermatology and Venereology : JEADV · 2026Article
- Computational discovery of precision therapeutics for hidradenitis suppurativa.bioRxiv : the preprint server for biology · 2026Article
- Genome instability and crosstalk with the immune response.Genome medicine · 2025Review
- Epidermal stem cells: skin surveillance and clinical perspective.Journal of translational medicine · 2024Review
- Reply to Nebo et al.: Pathogenesis of advanced hidradenitis suppurativa: Are there differences based on anatomical location, gender, and race?Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Upregulation of Caveolae-Associated Proteins in Lesional Samples of Hidradenitis Suppurativa: A Case Series Study.JID innovations : skin science from molecules to population health · 2023Article
- Overexpression of hypoxia-inducible factor-1α in hidradenitis suppurativa: the link between deviated immunity and metabolism.Archives of dermatological research · 2023Article
- Both cell autonomous and non-autonomous processes modulate the association between replication timing and mutation rate.Scientific reports · 2023Article
- Inborn Errors of Immunity in Hidradenitis Suppurativa Pathogenesis and Disease Burden.Journal of clinical immunology · 2023Review
- Cell-free DNA is elevated in the serum of patients with hidradenitis suppurativa.The Journal of dermatology · 2023Article
- Leveraging the replication stress response to optimize cancer therapy.Nature reviews. Cancer · 2023Review
- ARPC1B promotes mesenchymal phenotype maintenance and radiotherapy resistance by blocking TRIM21-mediated degradation of IFI16 and HuR in glioma stem cells.Journal of experimental & clinical cancer research : CR · 2022Article
- Advances in molecular pathogenesis of hidradenitis suppurativa: Dysregulated keratins and ECM signaling.Seminars in cell & developmental biology · 2022Review
- Holistic health record for Hidradenitis suppurativa patients.Scientific reports · 2022Article
- STING Signaling and Skin Cancers.Cancers · 2021Review
- Innate Immunity in Diabetic Wound Healing: Focus on the Mastermind Hidden in Chronic Inflammatory.Frontiers in pharmacology · 2021Review
- Sensing Stemness.Current stem cell reports · 2021Review
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hidradenitis suppurativa (HS) is a chronic, relapsing, inflammatory skin disease. HS appears to be a primary abnormality in the pilosebaceous-apocrine unit. In this work, we characterized hair follicle stem cells (HFSCs) isolated from HS patients and more precisely the outer root sheath cells (ORSCs). We showed that hair follicle cells from HS patients had an increased number of proliferating progenitor cells and lost quiescent stem cells. Remarkably, we also showed that the progression of replication forks was altered in ORSCs from hair follicles of HS patients, leading to activation of the ATR/CHK1 pathway. These alterations were associated with an increased number of micronuclei and with the presence of cytoplasmic ssDNA, leading to the activation of the IFI16/STING pathway and the production of type I IFNs. This mechanistic analysis of the etiology of HS in the HFSC compartment establishes a formal link between genetic predisposition and skin inflammation observed in HS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.