ArticleArthritis research & therapy2013
The severity of experimental arthritis is independent of IL-36 receptor signaling.
Article in Arthritis research & therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.
- Immunobiological Properties and Clinical Applications of Interleukin-38 for Immune-Mediated Disorders: A Systematic Review Study.International journal of molecular sciences · 2021Pooled it
- Advances in targeting IL-1 family cytokines for the treatment of inflammatory diseases.Nature reviews. Rheumatology · 2026Review
- Aged skin exacerbates experimental osteoarthritis via enhanced IL-36R signaling.Nature communications · 2026Article
- Role of IL-1 Family Cytokines IL-36, IL-37, IL-38 in Osteoarthritis and Rheumatoid Arthritis: A Comprehensive Review.Journal of inflammation research · 2024Review
- Role of Interleukin-36 in inflammatory joint diseases.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2023Review
- IL-36β promotes anti-tumor effects in CD8Annals of translational medicine · 2021Article
- IL-36 cytokines in inflammatory and malignant diseases: not the new kid on the block anymore.Cellular and molecular life sciences : CMLS · 2021Review
- Interleukin-36: Structure, Signaling and Function.Advances in experimental medicine and biology · 2021Review
- IL-38 and IL-36 Target Autophagy for Regulating Synoviocyte Proliferation, Migration, and Invasion in Rheumatoid Arthritis.Disease markers · 2021Article
- Protective effect of interleukin-36 receptor antagonist on liver injury induced by concanavalin A in mice.Iranian journal of basic medical sciences · 2020Article
- Interleukin-36 family dysregulation drives joint inflammation and therapy response in psoriatic arthritis.Rheumatology (Oxford, England) · 2020Article
- IL-38: A New Player in Inflammatory Autoimmune Disorders.Biomolecules · 2019Review
- TGF-β type 2 receptor-mediated modulation of the IL-36 family can be therapeutically targeted in osteoarthritis.Science translational medicine · 2019Article
- IL-36 Cytokines: Regulators of Inflammatory Responses and Their Emerging Role in Immunology of Reproduction.International journal of molecular sciences · 2019Review
- IL-36, IL-37, and IL-38 Cytokines in Skin and Joint Inflammation: A Comprehensive Review of Their Therapeutic Potential.International journal of molecular sciences · 2019Review
- Biology of IL-36 Signaling and Its Role in Systemic Inflammatory Diseases.Frontiers in immunology · 2019Review
- Function and Regulation of IL-36 Signaling in Inflammatory Diseases and Cancer Development.Frontiers in cell and developmental biology · 2019Review
- IL-36 cytokines in autoimmunity and inflammatory disease.Oncotarget · 2018Review
- Cytokines in the pathogenesis of rheumatoid arthritis: new players and therapeutic targets.BMC rheumatology · 2017Review
- Distinct expression of interleukin (IL)-36α, β and γ, their antagonist IL-36Ra and IL-38 in psoriasis, rheumatoid arthritis and Crohn's disease.Clinical and experimental immunology · 2016Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionInterleukin (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.
methodsCollagen-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.
resultsIL-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.
conclusionsThe development and severity of experimental arthritis are independent of IL-36R signaling.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.