IL-36γ Is Involved in Psoriasis and Allergic Contact Dermatitis

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IL-36γ Is Involved in Psoriasis and Allergic Contact Dermatitis Anna Balato, Martina Mattii, Giuseppina Caiazzo, Annunziata Raimondo, Cataldo Patruno, Nicola Balato, Fabio Ayala, Serena Lembo Journal of Investigative Dermatology Volume 136, Issue 7, Pages 1520-1523 (July 2016) DOI: 10.1016/j.jid.2016.03.020 Copyright © 2016 The Authors Terms and Conditions

Figure 1 IL-36 expression in psoriasis and allergic contact dermatitis. (a) IL-36 (α, β, and γ) and IL-36Ra (Ra) gene expression in lesional psoriatic skin (PSO, n = 20), lesional allergic contact dermatitis skin (ACD, n = 10), and healthy skin (HS, n = 10). (b) IL-36 gene expression in lesional skin of 10 psoriasis patients before and after 16 weeks of anti-TNF-α treatment. (c) IL-36γ serum levels in HC (n = 10), PSO (n = 10), and ACD (n = 10) subjects. Supernatants from healthy skin organ culture treated with TNF-α (20ng/ml) for 24 hours were used as positive controls (CTRL+). (d) IL-36γ gene expression in peripheral blood mononuclear cells (PBMCs) of HC (n = 5), PSO (n = 5), and ACD (n = 5) subjects. Data are displayed as mean ± standard deviation. ∗P < 0.05, ∗∗P < 0.01. 18S rRNA, 18S ribosomal RNA; ACD, allergic contact dermatitis; CTRL+, positive control; HS, healthy skin; PBMC, peripheral blood mononuclear cell; PSO, psoriatic skin; Ra, receptor antagonist; TNF, tumor necrosis factor. Journal of Investigative Dermatology 2016 136, 1520-1523DOI: (10.1016/j.jid.2016.03.020) Copyright © 2016 The Authors Terms and Conditions

Figure 2 Inflammatory cytokine gene expression in peripheral blood mononuclear cells (PBMCs) from whole study population and ex vivo ACD non lesional skin assay. (a) IL-36γ gene expression in PBMCs of 5 HC, 5 PSO, and 5 nickel-ACD subjects stimulated with concanavalin A (ConcA, 5μg/ml), toxic shock syndrome toxin (TSST-1, 100ng/ml), and nickel sulfate (NiSO4, 10−4 mol/L) for 24 hours. (b) IL-22 gene expression in PBMCs of 5 HC, 5 PSO, and 5 nickel-ACD subjects stimulated with TSST-1 (100ng/ml), NiSO4 (10−4 mol/L), and recombinant IL-36Ra (rIL-36Ra, 1.25 μg/mL) for 24 hours. (c) IL-36γ gene expression in healthy skin (HS, n = 5) and in non lesional (NLes) nickel-ACD skin (n = 5) stimulated with 30 mg of NiSO4 (5% in petrolatum). PBMCs isolated from the same subjects were incubated in the system with or without NiSO4. (d) IL-36γ, TNF-α, and IL-1α gene expression in PBMCs isolated from nickel-ACD subjects (n = 5) stimulated with NiSO4 (10−4 mol/L) and in PBMCs collected from ex vivo ACD NLes skin assay. Data are displayed as mean ± standard deviation. −, without treatment; +, with treatment. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001. 18S rRNA, 18S ribosomal RNA; ACD, allergic contact dermatitis; ConcA, concanavalin A; HC, healthy control; HS, healthy skin; PBMC, peripheral blood mononuclear cell; NLes, non lesional; PSO, psoriatic skin; rIL-36Ra, recombinant IL-36Ra; TNF, tumor necrosis factor; TSST-1, toxic shock syndrome toxin. Journal of Investigative Dermatology 2016 136, 1520-1523DOI: (10.1016/j.jid.2016.03.020) Copyright © 2016 The Authors Terms and Conditions