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

Autor: Franck Morel, Jérôme Amiaud, A. Bourreille, Marie-Astrid Boutet, Bénédicte Brulin, Céline Charrier, Maël Penhoat, M. Rolli‐Derkinderen, Frédéric Blanchard, B. Le Goff, Gaby Palmer, J.-C. Lecron, Géraldine Bart, Solenne Vigne, Cem Gabay
Přispěvatelé: maurice, sandrine, Physiopathologie des Adaptations Nutritionnelles (PhAN), Institut National de la Recherche Agronomique (INRA)-Université de Nantes (UN), Service de rhumatologie [Nantes], Université de Nantes (UN)-Hôtel-Dieu-Centre hospitalier universitaire de Nantes (CHU Nantes), Laboratoire Inflammation, Tissus épithéliaux et Cytokines (LITEC), Université de Poitiers, Service Immunologie/Inflammation [CHU Poitiers], Centre hospitalier universitaire de Poitiers (CHU Poitiers), Neuropathies du système nerveux entérique et pathologies digestives, implication des cellules gliales entériques, Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service d'hépato-gastroentérologie [CHU Nantes], Centre hospitalier universitaire de Nantes (CHU Nantes), Division of Rheumatology [Geneva, Switzerland], Geneva University Hospital, Geneva-Department of Internal Medicine Specialties [Geneva, Switzerland], This work was supported by Inserm, the Arthritis Foundation and by a grant from the Swiss National Science Foundation (310030_135195 to CG). M.A.B. was a recipient of a fellowship from the French Ministry of Research., Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Université de Genève (UNIGE), ROLLI-DERKINDEREN, MALVYNE, Université de Genève = University of Geneva (UNIGE)
Jazyk: angličtina
Rok vydání: 2016
Předmět:
0301 basic medicine
Keratinocytes
Male
rheumatoid arthritis
Arthritis
[SDV.IMM.II]Life Sciences [q-bio]/Immunology/Innate immunity
Arthritis
Rheumatoid
Mice
Crohn Disease
Immunology and Allergy
Macrophage
Medicine
Intestinal Mucosa
Skin
ddc:616
[SDV.MHEP.RSOA] Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal system
Imiquimod
[SDV.MHEP] Life Sciences [q-bio]/Human health and pathology
Synovial Membrane
Interleukin-36
Interleukin
psoriasis
3. Good health
Crohn's disease
[SDV.IMM.IA]Life Sciences [q-bio]/Immunology/Adaptive immunology
[SDV.MHEP.RSOA]Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal system
Mice
Inbred DBA
[SDV.IMM.IA] Life Sciences [q-bio]/Immunology/Adaptive immunology
Rheumatoid arthritis
Aminoquinolines
medicine.symptom
Immunology
Plasma Cells
Inflammation
Enzyme-Linked Immunosorbent Assay
Cell Line
03 medical and health sciences
Psoriasis
Animals
Humans
RNA
Messenger
[SDV.IMM.II] Life Sciences [q-bio]/Immunology/Innate immunity
business.industry
Interleukins
Macrophages
[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology
Dendritic Cells
Original Articles
[SDV.MHEP.DERM] Life Sciences [q-bio]/Human health and pathology/Dermatology
medicine.disease
Arthritis
Experimental
[SDV.MHEP.HEG] Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology
CCL20
Mice
Inbred C57BL
Disease Models
Animal
030104 developmental biology
IL-36
Th17 Cells
Caco-2 Cells
business
[SDV.MHEP.DERM]Life Sciences [q-bio]/Human health and pathology/Dermatology
[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Interleukin-1
Zdroj: Clinical and Experimental Immunology, Vol. 184, No 2 (2016) pp. 159-173
Clinical and Experimental Immunology
Clinical and Experimental Immunology, Wiley, 2016, 184 (2), pp.159-173. ⟨10.1111/cei.12761⟩
Clinical and experimental immunology
ISSN: 0009-9104
1365-2249
DOI: 10.1111/cei.12761⟩
Popis: Summary 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.
Databáze: OpenAIRE
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