ArticleProceedings of the National Academy of Sciences of the United States of America2016
Epipolymorphisms associated with the clinical outcome of autoimmune arthritis affect CD4+ T cell activation pathways.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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.
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Who cites it
14 citing papers in PubMed.
- Differential transcriptional and epigenetic signatures in CD4Journal of translational autoimmunity · 2026Article
- Stochastic epigenetic mutation profiles as biomarkers of clinical activity in juvenile idiopathic arthritis: a multi-omic machine learning approach for gene prioritization.Molecular medicine (Cambridge, Mass.) · 2025Article
- Single-cell landscape of immunological responses in patients with juvenile idiopathic arthritis.Genes & diseases · 2025Article
- Methylation of T and B Lymphocytes in Autoimmune Rheumatic Diseases.Clinical reviews in allergy & immunology · 2024Review
- Patterns and determinants of response to novel therapies in juvenile and adult-onset polyarthritis.Rheumatology (Oxford, England) · 2024Review
- Juvenile idiopathic arthritis.Nature reviews. Disease primers · 2022Review
- Review
- DNA methylation biomarkers of future health outcomes in children.Molecular and cellular pediatrics · 2020Review
- Immunome perturbation is present in patients with juvenile idiopathic arthritis who are in remission and will relapse upon anti-TNFα withdrawal.Annals of the rheumatic diseases · 2019Article
- Implications of juvenile idiopathic arthritis genetic risk variants for disease pathogenesis and classification.Current opinion in rheumatology · 2019Review
- Single-cell technologies - studying rheumatic diseases one cell at a time.Nature reviews. Rheumatology · 2019Review
- Targeting Tregs in Juvenile Idiopathic Arthritis and Juvenile Dermatomyositis-Insights From Other Diseases.Frontiers in immunology · 2019Review
- T Cell Receptor-Independent, CD31/IL-17A-Driven Inflammatory Axis Shapes Synovitis in Juvenile Idiopathic Arthritis.Frontiers in immunology · 2018Article
- New insights into the epigenetics of inflammatory rheumatic diseases.Nature reviews. Rheumatology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Multifactorial diseases, including autoimmune juvenile idiopathic arthritis (JIA), result from a complex interplay between genetics and environment. Epigenetic mechanisms are believed to integrate such gene-environment interactions, fine-tuning gene expression, and possibly contributing to immune system dysregulation. Although anti-TNF therapy has strongly increased JIA remission rates, it is not curative and up to 80% of patients flare upon treatment withdrawal. Thus, a crucial unmet medical and scientific need is to understand the immunological mechanisms associated with remission or flare to inform clinical decisions. Here, we explored the CD4
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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.