The balance between pro‐ and anti‐inflammatory cytokines is crucial in human allergic contact dermatitis pathogenesis: the role of IL‐1 family members. Issue 12 (December 2013)

• Record Type: Journal Article
• Authors: Mattii, Martina; Ayala, Fabio; Balato, Nicola; Filotico, Raffaele; Lembo, Serena; Schiattarella, Maria; Patruno, Cataldo; Marone, Gianni; Balato, Anna
• Is Part Of: Experimental dermatology. Volume 22:Issue 12(2013:Dec.)
• Page Start: 813
• Page End: 819
• Publication Date: 2013-12
• Subjects: Dermatology -- Periodicals; 616.5
• DOI: 10.1111/exd.12272
• Languages: English
• ISSNs: 0906-6705

Abstract

<abstract abstract-type="main" id="exd12272-abs-0001"> <title>Abstract</title> <p>The interleukin (IL)‐1 family includes 11 members that are important in inflammatory processes. It includes various agonists and two antagonists, IL‐1Ra and IL‐36Ra. Our aim was to investigate whether the IL‐1 family is involved in allergic contact dermatitis (ACD). The expression of IL‐1 family members was evaluated by PCR and immunohistochemistry in the positive patch test reaction site (involved skin) and in the uninvolved skin of ACD patients. We also examined these cytokines in an <italic>ex vivo</italic> model of ACD. The antagonistic activity of IL‐36Ra was evaluated by injecting recombinant IL‐36Ra in uninvolved skin biopsies of ACD patients. IL‐1Ra and IL‐36Ra expression was quantified in mononuclear cells of nickel‐sensitized patients challenged <italic>in vitro</italic> with nickel. IL‐33 involvement in ACD was investigated by intra‐dermal injection of anti‐IL‐33 in the uninvolved skin of patients <italic>ex vivo</italic>. Results showed that IL‐1β, IL‐1Ra, IL‐36α, IL‐36β, IL‐36γ and IL‐33 expression, but not IL‐36Ra expression, was enhanced in ACD‐involved skin. Immunohistochemical analysis and <italic>ex vivo</italic> skin cultures confirmed these results. Injection of anti‐IL‐33 in ACD‐uninvolved skin inhibited IL‐8 expression, whereas IL‐36Ra inhibited IL‐36α, IL‐36β, IL‐36γ and IL‐8 expression. Nickel induced IL‐1Ra expression in lymphocytes of nickel‐sensitized patients. Hence, various IL‐1 agonists and antagonists may be involved in ACD pathogenesis.</p> </abstract>