Distinct expression of interleukin (IL)-36α, β and γ, their antagonist IL-36Ra and IL-38 in psoriasis, rheumatoid arthritis and Crohn&#039;s disease

Boutet, M-A; Bart, G; Penhoat, M; Amiaud, J; Brulin, B; Charrier, C; Morel, F; Lecron, J-C; Rolli-Derkinderen, M; Bourreille, A; Vigne, Solenne; Gabay, Cem; Palmer-Lourenco, Gaby; Le Goff, B; Blanchard, F

doi:10.1111/cei.12761

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Title		Distinct expression of interleukin (IL)-36α, β and γ, their antagonist IL-36Ra and IL-38 in psoriasis, rheumatoid arthritis and Crohn's disease
Authors		Boutet, M-A Bart, G Penhoat, M Amiaud, J Brulin, B Charrier, C Morel, F Lecron, J-C Rolli-Derkinderen, M Bourreille, A Vigne, Solenne Gabay, Cem Palmer-Lourenco, Gaby Le Goff, B Blanchard, F show all authors [1 - 15]
Published in		Clinical and Experimental Immunology. 2016, vol. 184, no. 2, p. 159-173
Abstract		Interleukin (IL)-36α, IL-36β and IL-36γ are expressed highly in skin and are involved in the pathogenesis of psoriasis, while the antagonists IL-36Ra or IL-38, another potential IL-36 inhibitor, limit uncontrolled inflammation. The expression and role of IL-36 cytokines in rheumatoid arthritis (RA) and Crohn's disease (CD) is currently debated. Here, we observed that during imiquimod-induced mouse skin inflammation and in human psoriasis, expression of IL-36α, γ and IL-36Ra, but not IL-36β and IL-38 mRNA, was induced and correlated with IL-1β and T helper type 17 (Th17) cytokines (IL-17A, IL-22, IL-23, CCL20). In mice with collagen-induced arthritis and in the synovium of patients with RA, IL-36α, β, γ, IL-36Ra and IL-38 were all elevated and correlated with IL-1β, CCL3, CCL4 and macrophage colony-stimulating factor (M-CSF), but not with Th17 cytokines. In the colon of mice with dextran sulphate sodium-induced colitis and in patients with CD, only IL-36α, γ and IL-38 were induced at relatively low levels and correlated with IL-1β and IL-17A. We suggest that only a minor subgroup of patients with RA (17-29%) or CD (25%) had an elevated IL-36 agonists/antagonists ratio, versus 93% of patients with psoriasis. By immunohistochemistry, IL-36 cytokines were produced by various cell types in skin, synovium and colonic mucosa such as keratinocytes, CD68⁺ macrophages, dendritic/Langerhans cells and CD79α⁺ plasma cells. In primary cultures of monocytes or inflammatory macrophages (M1), IL-36β and IL-36Ra were produced constitutively, but IL-36α, γ and IL-38 were produced after lipopolysaccharide stimulation. These distinct expression profiles may help to explain why only subgroups of RA and CD patients have a potentially elevated IL-36 agonists/antagonists ratio.
Identifiers		DOI: 10.1111/cei.12761 PMID: 26701127
Full text		Article (Published version) (1.1 MB) - Limited access to UNIGE
Structures		Faculté de médecine / Section de médecine clinique / Département de médecine
Research groups		Mécanisme de l'inflammation articulaire (44) Biologie des cytokines de la famille de l'interleukine-1 (1022)
Citation (ISO format)		BOUTET, M-A et al. Distinct expression of interleukin (IL)-36α, β and γ, their antagonist IL-36Ra and IL-38 in psoriasis, rheumatoid arthritis and Crohn's disease. In: Clinical and Experimental Immunology, 2016, vol. 184, n° 2, p. 159-173. doi: 10.1111/cei.12761 https://archive-ouverte.unige.ch/unige:88666