ReviewAnnals of the rheumatic diseases2000
Arguments for interleukin 1 as a target in chronic arthritis.
Review in Annals of the rheumatic diseases, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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
18 citing papers in PubMed, 88 citations in OpenAlex.
- Innate immuno-response to nanoparticle uptake in liver and spleen mimics pathogen infection.Nanomedicine (London, England) · 2025Article
- High levels of TDO2 in relation to pro-inflammatory cytokines in synovium and synovial fluid of patients with osteoarthritis.BMC musculoskeletal disorders · 2022Article
- The role of annexin A1 in the modulation of the NLRP3 inflammasome.Immunology · 2020Article
- The caspase-8/RIPK3 signaling axis in antigen presenting cells controls the inflammatory arthritic response.Arthritis research & therapy · 2017Article
- Effects of Ezetimibe, Simvastatin, and their Combination on Inflammatory Parameters in a Rat Model of Adjuvant-Induced Arthritis.Inflammation · 2017Article
- Enhanced activity of NLRP3 inflammasome in peripheral blood cells of patients with active rheumatoid arthritis.Arthritis research & therapy · 2015Article
- Correlation between P2X7 receptor gene polymorphisms and gout.Rheumatology international · 2015Review
- Classical and Paradoxical Effects of TNF-α on Bone Homeostasis.Frontiers in immunology · 2014Review
- Targeting inflammasomes in rheumatic diseases.Nature reviews. Rheumatology · 2013Review
- Bone effects of biologic drugs in rheumatoid arthritis.Clinical & developmental immunology · 2013Review
- The Q705K polymorphism in NLRP3 is a gain-of-function alteration leading to excessive interleukin-1β and IL-18 production.PloS one · 2012Article
- Modulation of interleukin-1β-induced inflammatory responses by a synthetic cationic innate defence regulator peptide, IDR-1002, in synovial fibroblasts.Arthritis research & therapy · 2011Article
- Intratumor T helper type 2 cell infiltrate correlates with cancer-associated fibroblast thymic stromal lymphopoietin production and reduced survival in pancreatic cancer.The Journal of experimental medicine · 2011Article
- Polymorphisms in genes controlling inflammation and tissue repair in rheumatoid arthritis: a case control study.BMC medical genetics · 2011Article
- Autoimmune hepatitis: new paradigms in the pathogenesis, diagnosis, and management.Hepatology international · 2010Article
- Multiple interleukin-1beta-converting enzymes contribute to inflammatory arthritis.Arthritis and rheumatism · 2009Article
- Gene polymorphisms and pharmacogenetics in rheumatoid arthritis.Current genomics · 2008Article
- Novel insights in the regulation of CCL18 secretion by monocytes and dendritic cells via cytokines, toll-like receptors and rheumatoid synovial fluid.BMC immunology · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumour necrosis factor (TNF) and interleukin 1 (IL1) are considered as master cytokines in chronic, destructive arthritis. Therapeutic approaches in rheumatic arthritis (RA) patients so far mainly focused on TNF. Although TNF is a major inflammatory mediator in RA and a potent inducer of IL1, anti-TNF treatment is not effective in all patients, nor does it fully control the arthritic process in affected joints of good responders. Analysis of cytokine patterns in early synovial biopsy specimens of RA patients reveals prominent TNF staining in 50% of the patients, whereas IL1b staining was evident in 100%. This argues that TNF independent IL1 production occurs in some of the patients. Studies in a range of experimental arthritis models in mice make it clear that TNF is involved in early joint swelling. However, TNF alone is not arthritogenic nor destructive and exerts its arthritogenic potential through IL1 induction. Intriguingly, TNF independent IL1 production is found in many models. Its relevance is further underlined by the greater efficacy of anti-IL1 treatment as compared with anti-TNF treatment and the total lack of chronic, erosive arthritis in IL1b deficient mice. IL1b is not necessarily involved in early joint swelling, but is a crucial mediator in chronic arthritis and cartilage erosion in all models studied so far. This makes ILb an attractive target in chronic, destructive arthritis.
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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.