ArticleBMC medical genetics2018
Genetically determined high activities of the TNF-alpha, IL23/IL17, and NFkB pathways were associated with increased risk of ankylosing spondylitis.
Article in BMC medical genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04399382 (A Clinical Study Using Damage-associated Molecular Pattern and Apparent Diffusion Coefficient to Evaluate the Efficacy of Biologics for Treating Spondyloarthritis), which is not on this map. Cited by 43 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.
A Clinical Study Using Damage-associated Molecular Pattern and Apparent Diffusion Coefficient to Evaluate the Efficacy of Biologics for Treating Spondyloarthritis
Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.
- The association of polymorphisms in TNF and ankylosing spondylitis in common population: a meta-analysis.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2021Pooled it
- Immune Regulatory Endotypes Defined by TRIM-Dependent Ubiquitin Signaling and IFN-NF-κB Network Activity in Ankylosing Spondylitis.International journal of molecular sciences · 2026Article
- Multidrug-ResistantMicroorganisms · 2026Article
- Identification of an IL17RC missense variant in a Chinese family with multiple osteochondromas and ankylosing spondylitis.Journal of human genetics · 2025Article
- Analysis of immune cell infiltration landscape and identification of diagnostic biomarkers in ankylosing spondylitis.APL bioengineering · 2025Article
- Cohort profile: Copenhagen Hospital Biobank-chronic inflammatory disease-inflammatory bowel disease (CHB-CID:IBD) genetic cohort.European journal of epidemiology · 2025Article
- Review
- Proteomic Profiling of Inflammatory Protein Dysregulation in HLA-B27-Positive Ankylosing Spondylitis: Molecular Signatures and Potential Biomarkers.Biomolecules · 2025Article
- Reduced Bone Quality of Sacrum and Lumbal Vertebrae Spongiosa in Toll-like Receptor 2- and Toll-like Receptor 4-Knockout Mice: A Blinded Micro-Computerized Analysis.Biomolecules · 2025Article
- Human spinal enthesis comparative biology of IL-17F and IL-17A reveals greater T-cell IL-17F induction and IL-23 regulation.Frontiers in immunology · 2025Article
- A Multitrait Analysis of Genome-Wide Association Study Reveals the Shared Genetic Architecture Between Inflammatory Bowel Disease and Ankylosing Spondylitis.Mediators of inflammation · 2025Article
- The Long Noncoding RNA, LOC645166, in T Cells of Ankylosing Spondylitis (AS) Patients Regulates the FOXP3 Expression via the Axis of LOC645166/miR-188-5p/NFKBID.Mediators of inflammation · 2025Article
- Article
- Environmental and Genetic Determinants of Ankylosing Spondylitis.International journal of molecular sciences · 2024Review
- Functional genomics implicates natural killer cells in the pathogenesis of ankylosing spondylitis.medRxiv : the preprint server for health sciences · 2024Article
- Human Amniotic MSC Response in LPS-Stimulated Ascites from Patients with Cirrhosis: FOXO1 Gene and Th17 Activation in Enhanced Antibacterial Activation.International journal of molecular sciences · 2024Article
- Article
- Precision medicine in axial spondyloarthritis: current opportunities and future perspectives.Therapeutic advances in musculoskeletal disease · 2024Review
- Exploring hub pyroptosis-related genes, molecular subtypes, and potential drugs in ankylosing spondylitis by comprehensive bioinformatics analysis and molecular docking.BMC musculoskeletal disorders · 2023Article
- Genetic factors involved in the co‑occurrence of endometriosis with ankylosing spondylitis (Review).Molecular medicine reports · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 12 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAnkylosing spondylitis (AS) results from the combined effects of susceptibility genes and environmental factors. Polymorphisms in genes regulating inflammation may explain part of the heritability of AS.
methodsUsing a candidate gene approach in this case-control study, 51 mainly functional single nucleotide polymorphisms (SNPs) in genes regulating inflammation were assessed in 709 patients with AS and 795 controls. Data on the patients with AS were obtained from the DANBIO registry where patients from all of Denmark are monitored in routine care during treatment with conventional and biologic disease modifying anti-rheumatic drugs (bDMARDs). The results were analyzed using logistic regression (adjusted for age and sex).
resultsNine polymorphisms were associated with risk of AS (p < 0.05). The polymorphisms were in genes regulating a: the TNF-α pathway (TNF -308 G > A (rs1800629), and - 238 G > A (rs361525); TNFRSF1A -609 G > T (rs4149570), and PTPN22 1858 G > A (rs2476601)), b: the IL23/IL17 pathway (IL23R G > A (rs11209026), and IL18-137 G > C (rs187238)), or c: the NFkB pathway (TLR1 743 T > C (rs4833095), TLR4 T > C (rs1554973), and LY96-1625 C > G (rs11465996)). After Bonferroni correction the homozygous variant genotype of TLR1 743 T > C (rs4833095) (odds ratios (OR): 2.59, 95% confidence interval (CI): 1.48-4.51, p = 0.04), and TNFRSF1A -609 G > T (rs4149570) (OR: 1.79, 95% CI: 1.31-2.41, p = 0.01) were associated with increased risk of AS and the combined homozygous and heterozygous variant genotypes of TNF -308 G > A (rs1800629) (OR: 0.56, 95% CI: 0.44-0.72, p = 0.0002) were associated with reduced risk of AS.
conclusionWe replicated associations between AS and the polymorphisms in TNF (rs1800629), TNFRSF1A (rs4149570), and IL23R (rs11209026). Furthermore, we identified novel risk loci in TNF (rs361525), IL18 (rs187238), TLR1 (rs4833095), TLR4 (rs1554973), and LY96 (rs11465996) that need validation in independent cohorts. The results suggest that genetically determined high activity of the TNF-α, IL23/IL17, and NFkB pathways increase risk of AS.
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.