SynthesisThe Journal of rheumatology2012
Independent replication and meta analysis of association studies establish TNFSF4 as a susceptibility gene preferentially associated with the subset of anticentromere-positive patients with systemic sclerosis.
Synthesis in The Journal of rheumatology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
What it found
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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
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Unfolding the pathogenesis of scleroderma through genomics and epigenomics.Journal of autoimmunity · 2017Pooled it
- Immunogenetics of Systemic Sclerosis.Genes · 2024Review
- Association ofHeliyon · 2024Article
- Updates on genetics in systemic sclerosis.Inflammation and regeneration · 2021Review
- Classical Disease-Specific Autoantibodies in Systemic Sclerosis: Clinical Features, Gene Susceptibility, and Disease Stratification.Frontiers in medicine · 2020Review
- Article
- The Ox40/Ox40 Ligand Pathway Promotes Pathogenic Th Cell Responses, Plasmablast Accumulation, and Lupus Nephritis in NZB/W F1 Mice.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Article
- TNFSF4 Gene Variations Are Related to Early-Onset Autoimmune Thyroid Diseases and Hypothyroidism of Hashimoto's Thyroiditis.International journal of molecular sciences · 2016Article
- OX40L blockade protects against inflammation-driven fibrosis.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- OX40, OX40L and Autoimmunity: a Comprehensive Review.Clinical reviews in allergy & immunology · 2016Review
- Genetics of systemic sclerosis: recent advances.Current opinion in rheumatology · 2015Review
- Genetics of systemic sclerosis.Seminars in immunopathology · 2015Review
- Genetics, Epigenetics, and Genomics of Systemic Sclerosis.Rheumatic diseases clinics of North America · 2015Review
- Recent advances in the genetics of systemic sclerosis: toward biological and clinical significance.Current rheumatology reports · 2015Review
- Pathogenesis of Systemic Sclerosis.Frontiers in immunology · 2015Review
- The genetics of scleroderma: looking into the postgenomic era.Current opinion in rheumatology · 2012Review
Corrections and comments
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Authors and funding
30 authors at 14 institutions in 4 countries.
Funding
Abstract
objectiveIndependent replication with large cohorts and metaanalysis of genetic associations are necessary to validate genetic susceptibility factors. The known tumor necrosis factor (ligand) superfamily, member 4 gene (TNFSF4) systemic lupus erythematosus (SLE) risk locus has been found to be associated with systemic sclerosis (SSc) in 2 studies, but with discrepancies between them for genotype-phenotype correlation. Our objective was to validate TNFSF4 association with SSc and determine the subset with the higher risk.
methodsKnown SLE and SSc TNFSF4 susceptibility variants (rs2205960, rs1234317, rs12039904, rs10912580, and rs844648) were genotyped in 1031 patients with SSc and 1014 controls of French white ancestry. Genotype-phenotype association analysis and meta analysis of available data were performed, providing a population study of 4989 patients with SSc and 4661 controls, all of European white ancestry.
resultsAllelic and genotypic associations were observed for the 5 single-nucleotide polymorphisms (SNP) with the subset of patients with SSc who are positive for anticentromere antibodies (ACA) and only a trend for association with SSc and limited cutaneous SSc. Rs2205960 exhibited the strongest allelic association in ACA+ patients with SSc [p = 0.0015; OR 1.37 (1.12-1.66)], with significant intra-cohort association when compared to patients with SSc positive for ACA. Metaanalysis confirmed overall association with SSc but also raised preferential association with the ACA+ subset and strongest effect with rs2205960 [T allele p = 0.00013; OR 1.33 (1.15-1.54) and TT genotype p = 0.00046; OR 2.02 (1.36-2.98)].
conclusionWe confirm TNFSF4 as an SSc susceptibility gene and rs2205960 as a putative causal variant with preferential association in the ACA+ SSc subphenotype.
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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.