Rahel Thomi1, Simone Cazzaniga1,2,3, S Morteza Seyed Jafari1, Christoph Schlapbach1, Robert E Hunger1. 1. Department of Dermatology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland. 2. Centro Studi GISED, Bergamo, Italy. 3. Graduate School for Cellular and Biomedical Sciences, University of Bern, Bern, Switzerland.
Abstract
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.
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.
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