The precise pathogenic mechanisms in the development, persistence and worsening of hidradenitis suppurativa (HS) remain ill-defined. This chronic inflammatory dermatosis displays a strong Th1 and Th17 inflammatory signature with elevated levels of TNF-α, IL-1β, IL-17 and IFNγ in lesional and perilesional tissue. HS significantly differs to other chronic inflammatory dermatoses due to the development of hypertrophic scarring and dermal tunnels. The development of scarring and tunnels suggests that fibroblastic stromal cells (including myofibroblasts, fibroblasts, pericytes etc) may be involved in the development and progression of disease. Heterogeneous populations of fibroblasts have been identified in other inflammatory disorders and malignancy which contribute to inflammation and present novel therapeutic targets for fibrotic disorders. Findings in HS are consistent with these fibroblast subpopulations and may contribute to tunnel formation, aggressive squamous cell carcinoma and the phenotypic presentation of familial HS variants. We describe the existing knowledge regarding these mechanistic pathways and methods to confirm their involvement in the pathogenesis of HS. K E Y W O R D S acne inversa, fibroblasts, hidradenitis suppurativa, pathogenesis, scarring | 887 FREW Et al.
words)Hidradenitis suppurativa (HS) is a severe chronic inflammatory skin disease affecting human apocrine sweat gland-bearing skin regions. One unique feature of HS is the development of keratinized sinus tracts that grow extensively deep in the dermis and are highly immunogenic. Here, we demonstrated that the stem cell fate infidelity exists in the HS sinus tracts, which exhibit features of both surface epidermis and appendages. Using single cell transcriptome analyses, we finely dissected different compartments of the HS epithelium and identified their respective changes in cytokine expression during disease progression and the critical interactions with the immune cells. Together, our work provides advanced understanding of the pathological epidermal remodeling and important implications for HS therapeutics.
The Dermatology Life Quality Index (DLQI) is commonly used to measure health-related quality-of-life (QoL) in adults with skin diseases. Among patients with psoriasis, racial/ethnic minority patients were found to report higher DLQI scores, indicating greater QoL impact, than Non-Hispanic (NH) White patients. We aimed to determine whether DLQI scores differ by race/ethnicity among adults with atopic dermatitis (AD). We performed a cross-sectional study using data from the Atopic Dermatitis in America online survey. The study included adults who met age-modified United Kingdom Working Party Criteria for AD. The primary outcome was continuous DLQI score. Racial/ethnic categories were NH White [reference], NH Black, Hispanic, and NH other. Multivariable linear regression was performed to evaluate
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