Author(s): Thomi R, Cazzaniga S, Seyed Jafari SM, Schlapbach C, Hunger RE
Importance: In spite of progress in understanding the mechanisms underlying hidradenitis suppurativa (HS) as an inflammatory skin disease, there is still a demand for an overview on immunopathogenesis of HS.
Objective: To demonstrate the importance of the type 1/type 17 immune response in lesional HS skin by drawing a semantic connectivity map.
Design, Setting, and Participants: Single-center case series of 24 patients with HS. Association of HS with T helper 1/T helper 17 (TH1/TH17) phenotype was assessed using semantic map analysis.
Main Outcomes and Measures: Association of HS with TH1/TH17 phenotype.
Results: The analysis was performed on 24 lesional HS biopsy samples from untreated patients with HS (16 [67%] female; median age, 36.5 years [range, 21-51 years]) with a mean (SD) Hurley stage of 2.29 (0.62) and 9 punch biopsy samples from healthy controls (6 [67%] female; median age, 43 years [range, 23-66 years]). The map shows a clustering of all TH1/TH17-associated cytokines (interleukin 17 [IL-17], interferon γ, IL-12, IL-23, IL-32, IL-1β, tumor necrosis factor) around overall lesional inflammation. Tumor necrosis factor, IL-12, and IL-17 are even directly connected via interferon γ. In contrast, IL-13, a TH2-associated cytokine, was inversely correlated with the presence of TH1/TH17-associated cytokines, further highlighting the importance of the TH1/TH17 cytokines in HS pathogenesis.
Conclusions and Relevance: These findings suggest that HS may be a TH1/TH17-driven inflammatory skin disease.
Dermatology Journal and/or Publisher
Journal Name: JAMA dermatology
Journal Abbreviation: JAMA Dermatol
Journal Date Published:
National Center for Biotechnology Information
Article Source: http://www.ncbi.nlm.nih.gov/pubmed/29617527
Lasted Revision: 2018-04-04
Abstract Source: National Center for Biotechnology Information, U.S. National Library of Medicine Abstract Query for Hidradenitis suppurativa (HS).
Tags: Inflammatory Phenotypes Skin Disease TH1/TH17