Advances in Molecular Pathogenesis of Hidradenitis Suppurativa: Dysregulated Keratins and ECM Signaling
August 2022
in “
Seminars in cell & developmental biology
”
hidradenitis suppurativa keratins extracellular matrix LL-37 Th1 immune response Th17 immune response S100A8 S100A9 soluble interleukin 2 receptor hair follicle stem cell replication stress IFI16 STING neutrophil extracellular traps B cells type I interferons HS ECM IL-2 receptor Th1 Th17 S100 proteins interferons
TLDR Recent findings suggest that genetic factors, immune system issues, and skin cell defects might contribute to the development of hidradenitis suppurativa.
The document discusses recent advances in understanding the molecular pathogenesis of hidradenitis suppurativa (HS), emphasizing dysregulated keratins and extracellular matrix (ECM) signaling. Key points include the role of elevated antimicrobial peptide LL-37, Th1/Th17 immune response, and biomarkers like S100A8/A9 and soluble interleukin 2 receptor. It also examines hair follicle stem cell replication stress, IFI16/STING-dependent inflammation, and the contributions of neutrophil extracellular traps, B cells, and type I interferons to immune dysregulation in HS. These insights are essential for developing targeted therapeutic interventions.
