期刊
EXPERIMENTAL DERMATOLOGY
卷 28, 期 8, 页码 886-891出版社
WILEY
DOI: 10.1111/exd.13978
关键词
acne inversa; fibroblasts; hidradenitis suppurativa; pathogenesis; scarring
类别
资金
- National Center for Advancing Translational Sciences (NCATS) [UL1 TR001866]
- National Institutes of Health (NIH)
- Clinical and Translational Science Award (CTSA) programme
- National Institute of General Medical Sciences of the NIH [T32GM007739]
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-alpha, IL-1 beta, IL-17 and IFN gamma 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.
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