ArticleArthritis & rheumatology (Hoboken, N.J.)2014
Disease activity in systemic lupus erythematosus correlates with expression of the transcription factor AT-rich-interactive domain 3A.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- A regulatory variant at 19p13.3 is associated with primary biliary cholangitis risk and ARID3A expression.Nature communications · 2023Pooled it
- Sjögren's patient subgroups identified through whole genome DNA methylation profiling.Arthritis research & therapy · 2026Article
- Inhibition of Macrophage ARID3A Alleviates Myocardial Ischemia-Reperfusion Injury After Heart Transplantation by Reducing THBS1/CD47 Signaling-Mediated Neutrophil Extracellular Traps Formation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- ARID3a from the ARID family: structure, role in autoimmune diseases and drug discovery.Acta pharmacologica Sinica · 2023Review
- Several genetic variants associated with systemic sclerosis in a Chinese Han population.Clinical rheumatology · 2023Article
- Virtual ChIP-seq: predicting transcription factor binding by learning from the transcriptome.Genome biology · 2022Article
- Deficiencies in the DNA Binding Protein ARID3a Alter Chromatin Structures Important for Early Human Erythropoiesis.ImmunoHorizons · 2021Article
- TLR engagement induces ARID3a in human blood hematopoietic progenitors and modulates IFNα production.Cellular immunology · 2020Article
- New Frontiers: ARID3a in SLE.Cells · 2019Review
- ARID3a gene profiles are strongly associated with human interferon alpha production.Journal of autoimmunity · 2019Article
- Bone Marrow-Derived Mesenchymal Stem Cells From Patients With Systemic Lupus Erythematosus Have a Senescence-Associated Secretory Phenotype Mediated by a Mitochondrial Antiviral Signaling Protein-Interferon-β Feedback Loop.Arthritis & rheumatology (Hoboken, N.J.) · 2017Article
- A genome-wide association study identifies six novel risk loci for primary biliary cholangitis.Nature communications · 2017Article
- A Role for the Transcription FactorFrontiers in immunology · 2017Article
- Expression and methylation data from SLE patient and healthy control blood samples subdivided with respect to ARID3a levels.Data in brief · 2016Article
- Human effector B lymphocytes express ARID3a and secrete interferon alpha.Journal of autoimmunity · 2016Article
- The Transcription Factor ARID3a Is Important for In Vitro Differentiation of Human Hematopoietic Progenitors.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Antibody Reactivity of B Cells in Lupus Patients with Increased Disease Activity and ARID3a Expression.Antibodies (Basel, Switzerland) · 2015Article
- Differential expression of the transcription factor ARID3a in lupus patient hematopoietic progenitor cells.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveSystemic lupus erythematosus (SLE) is a complex and multifactorial autoimmune disease with striking clinical, immunologic, and genetic heterogeneity, despite nearly ubiquitous antinuclear antibody (ANA) production. Multiple gene polymorphisms have been associated with the disease, but these individually account for only a very small percentage of overall SLE risk. In earlier studies, constitutive expression of the DNA-binding protein AT-rich-interactive domain 3A (ARID3a) in transgenic mouse B lymphocyte lineage cells led to spontaneous ANA production and preferential development of B cells associated with production of polyreactive antibodies. Therefore, we undertook this study to determine whether ARID3a was overexpressed in B lymphocytes of SLE patients and whether ARID3a expression was associated with disease severity.
methodsA cross-section of SLE patients, rheumatoid arthritis patients, and age- and sex-matched controls was analyzed longitudinally for lupus disease activity, numbers of ARID3a+ peripheral blood mononuclear B cells from multiple B cell subsets, and immunoglobulin and cytokine levels.
resultsFifty of 115 SLE patients (43%) had dramatically increased numbers of ARID3a+ B cells compared to healthy controls. ARID3a was not expressed in naive B cells of healthy controls, but was abundant in these precursors of antibody-secreting cells in SLE patients. Total numbers of ARID3a+ B cells correlated with increased disease activity as defined by SLE Disease Activity Index scores in individuals assessed at 3 time points.
conclusionThese findings identify B cell anomalies in SLE that allow stratification of patient samples based on ARID3a expression and implicate ARID3a as a potential marker of CD19+ B lymphocytes correlated with disease activity.
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