ReviewAnnals of the New York Academy of Sciences2019
Targeting tumor necrosis factor receptors in ankylosing spondylitis.
Review in Annals of the New York Academy of Sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 60 citations in OpenAlex.
- Safety, pharmacokinetics, preliminary efficacy, pharmacodynamics, and immunogenicity of QX002N, an anti-IL-17A monoclonal antibody, after short-term treatment of active ankylosing spondylitis.BMC pharmacology & toxicology · 2025Trial
- Biologic immunomodulators and spinal fusion: evidence, mechanisms, and perioperative considerations.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 · 2026Review
- Molecular role of developmentally regulated GTP-binding protein 1 in coordinating osteoclast and osteoblast differentiation during bone remodeling.Molecules and cells · 2026Article
- Immunization with detoxified TNFα elicits neutralizing antibodies and ameliorates inflammatory shock and autoimmune arthritis in mice.Frontiers in immunology · 2026Article
- Exploration of Multidimensional Treatment for Ankylosing Spondylitis: From Traditional Medications to Emerging Immune-Targeted Perspectives.International journal of general medicine · 2026Review
- Biologic and targeted synthetic therapies in ankylosing spondylitis: a pharmacological review.Frontiers in pharmacology · 2026Review
- Real-World Experience with an Adalimumab Biosimilar (ABP 501) in Patients with Rheumatoid Arthritis, Ankylosing Spondylitis, Psoriatic Arthritis and Psoriasis in Europe: Results from the Adelphi Disease Specific Programme.Rheumatology and therapy · 2025Article
- The Genetic Background of Ankylosing Spondylitis Reveals a Distinct Overlap with Autoimmune Diseases: A Systematic Review.Journal of clinical medicine · 2025Review
- JAK inhibition and axial spondyloarthritis: new steps on the path to understanding pathophysiology.Frontiers in immunology · 2025Review
- Anti-Osteoporosis Is Imperative in Prevention of Progress of Ankylosing Spondylitis.International journal of general medicine · 2025Article
- No causal relationship between ankylosing spondylitis and Parkinson's disease: Insights from Mendelian randomization studies.Heliyon · 2024Article
- Identification of necroptosis-related genes in ankylosing spondylitis by bioinformatics and experimental validation.Journal of cellular and molecular medicine · 2024Article
- Progranulinopathy: A diverse realm of disorders linked to progranulin imbalances.Cytokine & growth factor reviews · 2024Review
- The totality of evidence approach in the development of AVT02 (adalimumab), a biosimilar to Humira.Therapeutic advances in chronic disease · 2024Review
- Review
- Anti-TNF Therapy Regulates Phagosome Pathway by Inhibiting NCF4 Expression to Treat Ankylosing Spondylitis.Journal of musculoskeletal & neuronal interactions · 2023Article
- Extracellular matrix turnover biomarkers reflect pharmacodynamic effects and treatment response of adalimumab in patients with axial spondyloarthritis-results from two randomized controlled trials.Arthritis research & therapy · 2023Article
- Have Therapeutics Enhanced Our Knowledge of Axial Spondyloarthritis?Current rheumatology reports · 2023Review
- High Baseline Neutrophil-to-Lymphocyte Ratio Could Serve as a Biomarker for Tumor Necrosis Factor-Alpha Blockers and Their Discontinuation in Patients with Ankylosing Spondylitis.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Dual-specificity phosphatases 22-deficient T cells contribute to the pathogenesis of ankylosing spondylitis.BMC medicine · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Over the past two decades, considerable advances in our understanding of inflammatory and immune pathways have allowed for the growing use of targeted biologic therapy. Most notably, the introduction of tumor necrosis factor (TNF) inhibitors has dramatically changed the management of autoimmune inflammatory disorders, including ankylosing spondylitis (AS). Despite the efficacy of TNF inhibitors documented in multiple clinical trials, anti-TNF therapy in AS is far from foolproof; it is associated with serious adverse effects and limited response to therapy in some patients. Moreover, specific questions regarding the role of TNF as a mediator of AS remain unanswered. Therefore, additional efforts are needed in order to better understand the role of TNF in the pathogenesis of AS and to develop safer and more effective treatment strategies. The purpose of this review is to better the understanding of the physiologic and pathogenic roles of TNF signaling in the course of AS. Relevant TNF biology and novel approaches to TNF blockade in AS are discussed.
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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.