ReviewFrontiers in immunology2018
Genetics and Functional Genomics of Spondyloarthritis.
Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- The Genetic Contribution to Drug Response in Spondyloarthritis: A Systematic Literature Review.Frontiers in genetics · 2021Pooled it
- Exploratory Cytokine and Bone-Marker Patterns in a Proteoglycan-Induced Spondyloarthritis Mouse Model: Th1/Th2 Strain Comparison and TLR2/3/4 Knockout Readouts.International journal of molecular sciences · 2026Article
- Article
- An Immunosenescent CD8+ T Cell Subset in Patients with Axial Spondyloarthritis and Psoriatic Arthritis Links Spontaneous Motility to Telomere Shortening and Dysfunction.Arthritis & rheumatology (Hoboken, N.J.) · 2025Article
- Expanding the Genetic Framework: Insights into Non-HLA-B27 Contributions to Axial Spondylarthritis.Medicina (Kaunas, Lithuania) · 2025Article
- HLA-B5 prevalence in patients with spondyloarthritis and impact on disease phenotype: a multicentric case-control study.Rheumatology (Oxford, England) · 2025Observational
- Exploring the Pathogenesis of Spondylarthritis beyond HLA-B27: A Descriptive Review.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
- The Role of Aminopeptidase ERAP1 in Human Pathology-A Review.Current issues in molecular biology · 2024Review
- Precision medicine in axial spondyloarthritis: current opportunities and future perspectives.Therapeutic advances in musculoskeletal disease · 2024Review
- Emerging Concepts in Precision Medicine in Axial Spondyloarthritis.Current rheumatology reports · 2023Review
- Human Leukocyte Antigen B27-Negative Axial Spondyloarthritis: What Do We Know?ACR open rheumatology · 2023Review
- Large-Scale Genetic Correlation Analysis between Spondyloarthritis and Human Blood Metabolites.Journal of clinical medicine · 2023Article
- Janus Kinase Inhibitors: A New Tool for the Treatment of Axial Spondyloarthritis.International journal of molecular sciences · 2023Review
- Population genetics and external proficiency testing for HLA disease associations.Frontiers in genetics · 2023Review
- Both Disease Activity and HLA-B27 Status Are Associated With Gut Microbiome Dysbiosis in Spondyloarthritis Patients.Arthritis & rheumatology (Hoboken, N.J.) · 2023Article
- How Has Molecular Biology Enhanced Our Undertaking of axSpA and Its Management.Current rheumatology reports · 2023Review
- High population frequencies ofFrontiers in immunology · 2023Article
- Microbiota-assisted therapy for systemic inflammatory arthritis: advances and mechanistic insights.Cellular and molecular life sciences : CMLS · 2022Review
- FunctionalCells · 2022Article
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
No grant is acknowledged in the PubMed record.
Abstract
Spondyloarthritis (SpA) is a chronic inflammatory disorder with high heritability but with complex genetics. It encompasses several entities that share common clinical features. Most of the genetic studies in SpA have been restricted to ankylosing spondylitis (AS), the prototypical form of SpA. However, there is growing evidence of shared genetic background between all the SpA subtypes and also with some other immune-mediated diseases. The most important part of SpA heritability comes from the HLA-B27 allele in the major histocompatibility complex (MHC) that explains around 25% of the attributable heredity. Several other loci outside of the MHC have been shown to be involved in the disease. However, all these non-MHC loci explain only a small additional fraction of disease predisposition. Thus, a substantial fraction of SpA genetic basis remains poorly understood. Gene expression profiling is a complementary approach to elucidate the underlying mechanisms and pathways that drive the disease. Several expression profiling studies have been undertaken in SpA. However, results have been quite disappointing with little overlap between the studies largely due to the small sample sizes, resulting in limited power to discover small effects. In this review, we summarize current knowledge on genetic findings concerning SpA and we describe strategic approaches for identification of additional variants, with a focus on rare variants in familial forms. We also provide an overview of gene expression studies in SpA and discuss the possibilities offered by high-throughput RNA sequencing technologies, in particular in sorted cells. Finally, issues in establishing molecular mechanisms underlying genetic association hits and potential translational applications will be addressed.
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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 Socratic graph.