ArticleArthritis research & therapy2013
Disease severity in K/BxN serum transfer-induced arthritis is not affected by IL-33 deficiency.
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 21 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 37 citations in OpenAlex.
- Advances in targeting IL-1 family cytokines for the treatment of inflammatory diseases.Nature reviews. Rheumatology · 2026Review
- A novel small molecule KMU-11361 attenuates rheumatoid arthritis by mechanistic inhibition of the TAK1-NF-κB-NLRP3 axis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- IL-1 family cytokines in inflammation and immunity.Cellular & molecular immunology · 2025Review
- The role of interleukin-18 and interleukin-18 binding protein in K/BxN serum transfer-induced arthritis.Frontiers in immunology · 2023Article
- Profiling of Tregs across tissues reveals plasticity in ST2 expression and hierarchies in tissue-specific phenotypes.iScience · 2022Article
- Blocking Interleukin-33 Alleviates the Joint Inflammation and Inhibits the Development of Collagen-Induced Arthritis in Mice.Journal of immunology research · 2020Article
- An intrinsic role of IL-33 in TNature immunology · 2020Article
- The IL-1 family of cytokines and receptors in rheumatic diseases.Nature reviews. Rheumatology · 2019Review
- Anti-inflammatory and immune-regulatory cytokines in rheumatoid arthritis.Nature reviews. Rheumatology · 2019Review
- Pleiotropic Effects of IL-33 on CD4Frontiers in immunology · 2019Review
- Serum IL-33, a new marker predicting response to rituximab in rheumatoid arthritis.Arthritis research & therapy · 2016Observational
- Interleukin-33 in health and disease.Nature reviews. Immunology · 2016Review
- Collagen-induced arthritis and imiquimod-induced psoriasis develop independently of interleukin-33.Arthritis research & therapy · 2016Article
- Interleukin 33 is a guardian of barriers and a local alarmin.Nature immunology · 2016Review
- Interleukin-33 and RANK-L Interplay in the Alveolar Bone Loss Associated to Periodontitis.PloS one · 2016Article
- Atherosclerosis severity is not affected by a deficiency in IL-33/ST2 signaling.Immunity, inflammation and disease · 2015Article
- Epidermal Expression and Regulation of Interleukin-33 during Homeostasis and Inflammation: Strong Species Differences.The Journal of investigative dermatology · 2015Article
- Therapeutic effect of IVIG on inflammatory arthritis in mice is dependent on the Fc portion and independent of sialylation or basophils.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Role of IL-33 and its receptor in T cell-mediated autoimmune diseases.BioMed research international · 2014Article
- Emerging role of interleukin-33 in autoimmune diseases.Immunology · 2014Review
Corrections and comments
- Commented on by
Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionInterleukin (IL)-33 is a cytokine of the IL-1 family, which signals through the ST2 receptor. Previous work suggested implication of the IL-33/ST2 axis in the pathogenesis of human and mouse arthritis. Here, we directly investigated the role of endogenous IL-33 in K/BxN serum transfer-induced arthritis by using IL-33 knockout (KO) mice.
methodsArthritis was induced by injection of complete K/BxN serum or purified IgG. Disease severity was monitored by clinical and histological scoring.
resultsK/BxN serum transfer induced pronounced arthritis with similar incidence and severity in IL-33 KO and wild-type (WT) mice. In contrast, disease development was significantly reduced in ST2 KO mice. IL-33 expression in synovial tissue was comparable in arthritic WT and ST2 KO mice, and absent in IL-33 KO mice. Transfer of purified arthritogenic IgG instead of complete K/BxN serum also resulted in similar arthritis severity in IL-33 KO and WT mice, excluding a contribution of IL-33 contained in the serum of donor mice to explain this result. We investigated additional potential confounding factors, including purity of genetic background, but the mechanisms underlying reduced arthritis in ST2 KO mice remained unclear.
conclusionsThe data obtained with IL-33 KO mice indicate that endogenous IL-33 is not required for the development of joint inflammation in K/BxN serum transfer-induced arthritis. On the contrary, arthritis severity was reduced in ST2 KO mice. This observation might relate to IL-33 independent effects of ST2, and/or reveal the existence of confounding variables affecting the severity of joint inflammation in these KO strains.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.