Trial reportAnnals of the rheumatic diseases2017
Canakinumab reverses overexpression of inflammatory response genes in tumour necrosis factor receptor-associated periodic syndrome.
Trial report in Annals of the rheumatic diseases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01242813 (An Open-label, Multicenter, Efficacy and Safety Study of 4-month Canakinumab Treatment With 6-month Follow-up in Patients With Active Recurrent or Chronic TNF-receptor Associated Periodic Syndrome), which is not on this map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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.
An Open-label, Multicenter, Efficacy and Safety Study of 4-month Canakinumab Treatment With 6-month Follow-up in Patients With Active Recurrent or Chronic TNF-receptor Associated Periodic Syndrome (TRAPS).
Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- The 2021 EULAR/American College of Rheumatology Points to Consider for Diagnosis, Management and Monitoring of the Interleukin-1 Mediated Autoinflammatory Diseases: Cryopyrin-Associated Periodic Syndromes, Tumour Necrosis Factor Receptor-Associated Periodic Syndrome, Mevalonate Kinase Deficiency, and Deficiency of the Interleukin-1 Receptor Antagonist.Arthritis & rheumatology (Hoboken, N.J.) · 2022Pooled it
- White Blood Cells and Blood Pressure: A Mendelian Randomization Study.Circulation · 2020Trial
- Glial Cell Dynamics in Neuroinflammation: Mechanisms, Interactions, and Therapeutic Implications.Biomedicines · 2026Review
- Neuroinflammation: Mechanisms, Dual Roles, and Therapeutic Strategies in Neurological Disorders.Current issues in molecular biology · 2025Review
- A novel TNFRSF1A mutation associated with TNF-receptor-associated periodic syndrome and its metabolic signature.Rheumatology (Oxford, England) · 2023Article
- Neutrophils in COVID-19: Not Innocent Bystanders.Frontiers in immunology · 2022Review
- Trained Immunity Contribution to Autoimmune and Inflammatory Disorders.Frontiers in immunology · 2022Review
- Trained immunity as a possible newcomer in autoinflammatory and autoimmune diseases pathophysiology.Frontiers in medicine · 2022Review
- Peripheral white blood cell counts mediated the associations of sleep duration with atherosclerotic cardiovascular disease risk: a cross-sectional study of middle-aged and older Chinese.Sleep & breathing = Schlaf & Atmung · 2021Article
- Compromised Protein Prenylation as Pathogenic Mechanism in Mevalonate Kinase Deficiency.Frontiers in immunology · 2021Review
- Beneficial Effects of Inflammatory Cytokine-Targeting Aptamers in an Animal Model of Chronic Prostatitis.International journal of molecular sciences · 2020Article
- Revisiting TNF Receptor-Associated Periodic Syndrome (TRAPS): Current Perspectives.International journal of molecular sciences · 2020Review
- IL1α Antagonizes IL1β and Promotes Adaptive Immune Rejection of Malignant Tumors.Cancer immunology research · 2020Article
- Autophagy Modulation in Lymphocytes From COVID-19 Patients: New Therapeutic Target in SARS-COV-2 Infection.Frontiers in pharmacology · 2020Article
- Periodic fever syndromes and the autoinflammatory diseases (AIDs).Journal of translational autoimmunity · 2020Review
- Somatic mosaicism in adult-onset TNF receptor-associated periodic syndrome (TRAPS).Molecular genetics & genomic medicine · 2019Article
- Unveiling the Efficacy, Safety, and Tolerability of Anti-Interleukin-1 Treatment in Monogenic and Multifactorial Autoinflammatory Diseases.International journal of molecular sciences · 2019Review
- p300/CBP inhibitor A-485 alleviates acute liver injury by regulating macrophage activation and polarization.Theranostics · 2019Article
- Tumour necrosis factor signalling in health and disease.F1000Research · 2019Review
- Tumor necrosis factor-associated periodic syndrome in adults.Rheumatology international · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 8 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo explore whether gene expression profiling can identify a molecular mechanism for the clinical benefit of canakinumab treatment in patents with tumour necrosis factor receptor-associated periodic syndrome (TRAPS).
methodsBlood samples were collected from 20 patients with active TRAPS who received canakinumab 150 mg every 4 weeks for 4 months in an open-label proof-of-concept phase II study, and from 20 aged-matched healthy volunteers. Gene expression levels were evaluated in whole blood samples by microarray analysis for arrays passing quality control checks.
resultsPatients with TRAPS exhibited a gene expression signature in blood that differed from that in healthy volunteers. Upon treatment with canakinumab, many genes relevant to disease pathogenesis moved towards levels seen in the healthy volunteers. Canakinumab downregulated the TRAPS-causing gene (TNF super family receptor 1A (TNFRSF1A)), the drug-target gene (interleukin (IL)-1B) and other inflammation-related genes (eg, MAPK14). In addition, several inflammation-related pathways were evident among the differentially expressed genes. Canakinumab treatment reduced neutrophil counts, but the observed expression differences remained after correction for this.
conclusionsThese gene expression data support a model in which canakinumab produces clinical benefit in TRAPS by increasing neutrophil apoptosis and reducing pro-inflammatory signals resulting from the inhibition of IL-1β. Notably, treatment normalised the overexpression of TNFRSF1A, suggesting that canakinumab has a direct impact on the main pathogenic mechanism in TRAPS. TRIAL REGISTRATION NUMBER: NCT01242813.
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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.