Project description:This study investigated the underlying inflammatory pathways and cell types in hidradenitis suppurativa using transcriptomic approaches with RNA sequencing of lesional and non-lesional skin biopsies from hidradenitis suppurativa patients.
Project description:Hidradenitis suppurativa is a common, debilitating inflammatory skin disease linked to immune dysregulation and abnormalities in follicular structure and function. Few studies have characterized the transcriptomic profile of affected and unaffected skin. We established an RNA-Seq based hidradenitis suppurativa expression disease signature and found it largely concordant with an earlier microarray-based study. We confirmed known aspects of the underlying disease biology including known immune response pathways, differential regulation of antimicrobial peptides, and complement activation. We further characterize the extent of changes in the complement cascade in hidradenitis lesions and highlight a signature that implicates host response to bacteria in disease pathogenesis.
Project description:Hidradenitis suppurativa (HS) is an inflammatory skin disease with limited therapeutic options. We and others have previously identified an abnormal B cell infiltrate within HS lesional skin. We performed scRNASequencing on CD3 negative cells from inflammatory HS skin lesions, healthy control skin and matched blood to better understand infiltrating B cells amongst other immune cells within lesional skin.
Project description:Hidradenitis suppurativa (HS) is an inflammatory skin disease with limited therapeutic options. CD4 T Cells have been described as more inflammatory than T cells in healthy skin. To better understand alterations within the T cell compartment, we profiled CD4 Teffector cells and regulatory T cells (Treg) from inflammatory HS skin lesions and healthy control skin via scRNASequencing.
Project description:Hidradenitis Suppurativa molecular taxonomy and key signaling pathways were studied by whole transcriptome profiling. Dysregulated genes were detected by comparing lesional and non lesional skin obtained from female HS patients and matched healthy controls using the Agilent array platform
