The severity of experimental arthritis is independent of IL-36 receptor signaling

Lamacchia, Céline; Palmer-Lourenco, Gaby; Rodriguez, Emiliana; Martin, Praxedis Sina; Vigne, Solenne; Seemayer, Christian Alexander; Talabot-Ayer, Dominique; Towne, Jennifer E; Gabay, Cem

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Title		The severity of experimental arthritis is independent of IL-36 receptor signaling
Authors		Lamacchia, Céline Palmer-Lourenco, Gaby Rodriguez, Emiliana Martin, Praxedis Sina Vigne, Solenne Seemayer, Christian Alexander Talabot-Ayer, Dominique Towne, Jennifer E Gabay, Cem show all authors [1 - 9]
Published in		Arthritis Research and Therapy. 2013, vol. 15, no. 2, p. R38
Abstract		INTRODUCTION: Interleukin (IL)-36 refers to three related IL-1 family cytokines, IL-36α, IL-36β, and IL-36γ, that bind to the IL-36 receptor (IL-36R). IL-36 exerts proinflammatory effects in skin and lung and stimulates T cell responses. In the present study, we examined the expression and function of IL-36R and its ligands in experimental arthritis. METHODS: Collagen-induced arthritis (CIA), antigen-induced arthritis (AIA), and K/BxN serum transfer-induced arthritis were induced according to standard protocols. Messenger RNA levels for IL-36R and its ligands in the joints of mice with CIA were determined by RT-qPCR. Mice with CIA were injected with a blocking monoclonal anti-IL-36R, a blocking anti-IL-1RI, or their isotype-matched control antibodies at the time of arthritis onset. Anti-IL-36R or control antibodies were also injected at the time of AIA induction. Finally, IL-36R-deficient mice were examined in AIA and serum transfer-induced arthritis. The development and severity of arthritis were assessed by clinical and histological scoring. RESULTS: IL-36R, IL-36Ra and IL-36γ mRNA were detected in the joints of mice with CIA, but their levels did not correlate with arthritis severity. As opposed to anti-IL-1RI antibody treatment, the injection of an anti-IL-36R antibody was devoid of effect on the development and severity of CIA. The severity of joint inflammation and structural damage in AIA was also unaltered by anti-IL-36R antibody treatment. Finally, the severity of AIA and K/BxN serum transfer-induced arthritis was similar in IL-36R-deficient and wild-type mice. CONCLUSIONS: The development and severity of experimental arthritis are independent of IL-36R signaling.
Identifiers		DOI: 10.1186/ar4192 PMID: 23452551
Full text		Article (Published version) (624 Kb) - Free access
Structures		Faculté de médecine / Section de médecine clinique / Département de médecine interne des spécialités Faculté de médecine / Section de médecine fondamentale / Département de pathologie et immunologie Faculté de médecine / Section de médecine fondamentale / Département de physiologie cellulaire et métabolisme
Research group		Mécanisme de l'inflammation articulaire (44)
Citation (ISO format)		LAMACCHIA, Céline et al. The severity of experimental arthritis is independent of IL-36 receptor signaling. In: Arthritis Research and Therapy, 2013, vol. 15, n° 2, p. R38. https://archive-ouverte.unige.ch/unige:46004