ArticleJournal of immunology (Baltimore, Md. : 1950)2015
Cutting Edge: Chronic NF-κB Activation in CD4+ T Cells in Rheumatoid Arthritis Is Genetically Determined by HLA Risk Alleles.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 17 citations in OpenAlex.
- Distinct Interferon and Intracellular Signaling Signatures in Systemic Lupus Erythematosus and Dermatomyositis by Integrative Transcriptomic and Proteomic Analysis.ACR open rheumatology · 2026Article
- Rheumatoid arthritis-recent advances in pathogenesis and the anti-inflammatory effect of plant-derived COX inhibitors.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Genetic basis of defects in immune tolerance underlying the development of autoimmunity.Frontiers in immunology · 2022Review
- Genetic and environmental risk factors for rheumatoid arthritis.Best practice & research. Clinical rheumatology · 2017Review
- Inflammation and epigenetic regulation in osteoarthritis.Connective tissue research · 2017Review
- Update on the genetic architecture of rheumatoid arthritis.Nature reviews. Rheumatology · 2017Review
- Factors Associated With Pathogenicity of Anti-Glomerular Basal Membrane Antibodies: A Case Report.Medicine · 2016Article
- Collagen Specific T-Cell Repertoire and HLA-DR Alleles: Biomarkers of Active Refractory Rheumatoid Arthritis.EBioMedicine · 2015Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Of identified genetic variants, HLA polymorphisms confer the greatest risk for developing autoimmune diseases, including rheumatoid arthritis (HLA-DRB1*04). There are strong influences of HLA polymorphisms on cell type-specific gene expression in B cells and monocytes. Their influence on gene expression in CD4(+) T cells is not known. We determined transcript and proteins levels of target genes in lymphocyte/monocyte subsets in healthy controls and rheumatoid arthritis subjects as a function of HLA-DRB1*04 haplotype. We identified gene expression dependent on HLA-DRB1*04 genotype in CD4(+) T cells. NF-κB activity in CD4(+) T cells was also dependent on HLA-DRB1*04 genotype, and blocking HLA-DR inhibited NF-κB activity in CD4(+) T cells and normalized gene expression, as did pharmacologic inhibition of NF-κB. We conclude that interactions between TCR and MHC class II encoded by HLA-DRB1*04 create a proinflammatory "hum" altering CD4(+) T cell phenotype.
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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.