Cutaneous infiltration of plasmacytoid dendritic cells and T regulatory cells in skin lesions of polymorphic light eruption. (27th February 2018)

• Record Type: Journal Article
• Authors: Rossi, M.T.; Arisi, M.; Lonardi, S.; Lorenzi, L.; Ungari, M.; Serana, F.; Fusano, M.; Moggio, E.; Calzavara‐Pinton, P.G.; Venturini, M.
• Is Part Of: Journal of the European Academy of Dermatology and Venereology. Volume 32:Number 6(2018)
• Page Start: 985
• Page End: 991
• Publication Date: 2018-02-27
• Subjects: Dermatology -- Periodicals; Sexually transmitted diseases -- Periodicals; 616.5
• DOI: 10.1111/jdv.14866
• Languages: English
• ISSNs: 0926-9959

Abstract

Abstract: Background: Polymorphic light eruption (PLE) is the most common autoimmune photodermatosis. Plasmacytoid dendritic cells (PDCs) are important mediators of innate antimicrobial immunity involved in the pathogenesis of many inflammatory skin diseases. In addition to PDCs, regulatory T cells (Tregs) are involved in controlling inflammation and adaptive immunity in skin by their immunosuppressive capacity. Objective: The aim of this study was to investigate the presence of PDCs and Tregs in photoexposed skin from PLE compared to healthy skin. Methods: Patients with PLE diagnosis and healthy controls were recruited and underwent a photoprovocative test. A 4‐mm punch biopsy was taken from the site of positive photoprovocation test reaction, and immunohistochemistry for BDCA2 as marker for PDCs, CD4 and FOXP3 as markers for Tregs was performed. Double immunostain for FOXP3 and CD4 was performed as well. Absolute counts for CD4, BDCA2 and FOXP3 were performed in at least 5 High Power Fields (HPF). Percentage of CD4‐, BDCA2‐ and CD4FOXP3‐positive cells over the total inflammatory infiltrate was assessed for each case. Results: We enrolled 23 patients and controls. BDCA2+ cells were present in 91.3% of PLE skin samples and 100% of healthy volunteer. Both in PLE patients and healthy controls, PDCs distribution was mainly dermic ( P < 0.05). Compared to healthy controls, both epidermic and dermic BDCA2+ cells count were significantly higher in PLE patients ( P < 0.05). Both in PLE patients and healthy controls, Tregs distribution was mainly dermic ( P < 0.05). The presence of both CD4+ cells and FOXP3+ cells was significantly higher in the dermis of PLE patients compared to controls ( P < 0.05). Relative percentages of cellular infiltrations confirmed these results. Conclusions: D‐PDCS and Tregs may play a significant role in the development of PLE, and dermal distribution of PDCs in PLE skin biopsies seems to confirm a possible overlap with cutaneous lupus erythematosus (CLE).