Journal
ARTHRITIS RESEARCH & THERAPY
Volume 15, Issue 2, Pages -Publisher
BIOMED CENTRAL LTD
DOI: 10.1186/ar4192
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Funding
- Swiss National Science Foundation [310030_135195, 310030_134691]
- Rheumasearch Foundation
- Institute for Arthritis Research
- Swiss National Science Foundation (SNF) [310030_134691, 310030_135195] Funding Source: Swiss National Science Foundation (SNF)
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Introduction: Interleukin (IL)-36 refers to three related IL-1 family cytokines, IL-36 alpha, IL-36 beta, and IL-36 gamma, 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-36 gamma 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.
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