ReviewAnnals of the rheumatic diseases2007
Amplifying elements of arthritis and joint destruction.
Review in Annals of the rheumatic diseases, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 58 citations in OpenAlex.
- Anti-CD19 CAR T-cell therapy for autoimmune diseases: from exploratory clinical trials to quantitative pharmacodynamic modeling development.Frontiers in immunology · 2026Review
- Research progress on complications of rheumatoid arthritis.Frontiers in immunology · 2025Review
- Progress of linking gut microbiota and musculoskeletal health: casualty, mechanisms, and translational values.Gut microbes · 2023Review
- Prediction of Erosive Disease Development by Antimitochondrial Antibodies in Rheumatoid Arthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2023Article
- Key residues in TLR4-MD2 tetramer formation identified by free energy simulations.PLoS computational biology · 2019Article
- TLR4 rs41426344 increases susceptibility of rheumatoid arthritis (RA) and juvenile idiopathic arthritis (JIA) in a central south Chinese Han population.Pediatric rheumatology online journal · 2017Article
- TLRs, future potential therapeutic targets for RA.Autoimmunity reviews · 2017Review
- A benzamide-linked small molecule NDMC101 inhibits NFATc1 and NF-κB activity: a potential osteoclastogenesis inhibitor for experimental arthritis.Journal of clinical immunology · 2012Article
- A profile of immune response to herpesvirus is associated with radiographic joint damage in rheumatoid arthritis.Arthritis research & therapy · 2012Article
- Anti-Arthritic and Analgesic Effect of NDI10218, a Standardized Extract of Terminalia chebula, on Arthritis and Pain Model.Biomolecules & therapeutics · 2012Article
- Trapped in a vicious loop: Toll-like receptors sustain the spontaneous cytokine production by rheumatoid synovium.Arthritis research & therapy · 2011Article
- Murine visceral leishmaniasis: IgM and polyclonal B-cell activation lead to disease exacerbation.European journal of immunology · 2010Article
- Translational mini-review series on Th17 cells: are T helper 17 cells really pathogenic in autoimmunity?Clinical and experimental immunology · 2010Review
- Hypothyroidism in Noninterferon Treated-HCV Infected Individuals Is Associated with Abnormalities in the Regulation of Th17 Cells.Hepatitis research and treatment · 2010Article
- Cytokine networks in systemic lupus erythematosus.Journal of biomedicine & biotechnology · 2010Review
- Local interleukin-1-driven joint pathology is dependent on toll-like receptor 4 activation.The American journal of pathology · 2009Article
- IL-17 as a future therapeutic target for rheumatoid arthritis.Nature reviews. Rheumatology · 2009Review
- Therapeutic targeting of Toll-like receptors for infectious and inflammatory diseases and cancer.Pharmacological reviews · 2009Review
- Dichloroacetate alleviates development of collagen II-induced arthritis in female DBA/1 mice.Arthritis research & therapy · 2009Article
- Infliximab in the treatment of rheumatoid arthritis.Biologics : targets & therapy · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rheumatoid arthritis (RA) is a systemic autoimmune disease characterised by chronic joint inflammation and variable degrees of bone and cartilage erosion. Studies in animal models of arthritis provide insight into elements which can amplify destructive features. The presence of immune complexes in the joint makes arthritis more erosive. Although considerable bone erosion still occurs in the absence of FcgammaR triggering by immune complexes, through cytokine-induced RANKL and direct osteoclast activation, cartilage erosion is heavily dependent on the FcgammaR pathway. T cell factors such as IFNgamma and IL17 further amplify erosion through upregulation of the damaging FcgammaRI and stimulation of the influx of granulocytes, respectively. Apart from immune elements, environmental pressure and components of tissue damage contribute through innate pathways. Spontaneous T cell-dependent arthritis in IL1Ra-/- mice is absent under germ-free conditions, and markedly suppressed in TLR4-deficient mice. Moreover, TLR4 blocking with a receptor antagonist suppresses erosive arthritis.
Indexed as
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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.