ReviewAutoimmunity2014
The complex role of DNA, histones and HMGB1 in the pathogenesis of SLE.
Review in Autoimmunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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
26 citing papers in PubMed, 52 citations in OpenAlex.
- Vagus nerve control of HMGB1 accessibility: a bioelectronic strategy for inflammation and pain.Bioelectronic medicine · 2026Review
- CpG-A induces liquid-liquid phase separation of HMGB1 to activate the RAGE-mediated inflammatory pathway.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The greatest contribution to medical science is the transformation from studying symptoms to studying their causes-the unrelenting legacy of Robert Koch and Louis Pasteur-and a causality perspective to approach a definition of SLE.Frontiers in immunology · 2024Article
- The role of circulating cell-free DNA as an inflammatory mediator after stroke.Seminars in immunopathology · 2023Review
- Receptor for Advanced Glycation End Products (RAGE): A Pivotal Hub in Immune Diseases.Molecules (Basel, Switzerland) · 2022Review
- HMGB1 is a critical molecule in the pathogenesis of Gram-negative sepsis.Journal of intensive medicine · 2022Review
- Type I Interferon Response Is Mediated by NLRX1-cGAS-STING Signaling in Brain Injury.Frontiers in molecular neuroscience · 2022Article
- Autoantibody-mediated impairment of DNASE1L3 activity in sporadic systemic lupus erythematosus.The Journal of experimental medicine · 2021Article
- Circulating Free DNA and Its Emerging Role in Autoimmune Diseases.Journal of personalized medicine · 2021Review
- The Anti-DNA Antibodies: Their Specificities for Unique DNA Structures and Their Unresolved Clinical Impact-A System Criticism and a Hypothesis.Frontiers in immunology · 2021Review
- Plasma Nucleosomes in Primary Breast Cancer.Cancers · 2020Article
- Increased serum calpain activity is associated with HMGB1 levels in systemic sclerosis.Arthritis research & therapy · 2020Article
- Psoriasis and systemic lupus erythematosus in children - literature review based on case report.Reumatologia · 2020Article
- HMGB1 in Systemic Lupus Erythematosus.Frontiers in immunology · 2020Review
- Extracellular HMGB-1 activates inflammatory signaling in tendon cells and tissues.Therapeutic advances in chronic disease · 2020Article
- Autoimmunity and SLE: Factual and Semantic Evidence-Based Critical Analyses of Definitions, Etiology, and Pathogenesis.Frontiers in immunology · 2020Review
- Johnny on the Spot-Chronic Inflammation Is Driven by HMGB1.Frontiers in immunology · 2019Review
- AGER-Mediated Lipid Peroxidation Drives Caspase-11 Inflammasome Activation in Sepsis.Frontiers in immunology · 2019Article
- The dsDNA, Anti-dsDNA Antibody, and Lupus Nephritis: What We Agree on, What Must Be Done, and What the Best Strategy Forward Could Be.Frontiers in immunology · 2019Review
- Epichromatin and chromomeres: a 'fuzzy' perspective.Open biology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterized by the production of antinuclear antibodies (ANA) in association with protean clinic manifestations. ANA can bind to nuclear molecules, most prominently DNA and histones in nucleosomes, to form complexes to promote pathogenesis. Because of the intrinsic immunological activity of the nuclear components, these complexes can amplify responses by interacting with diverse pattern recognition receptors and internal sensing systems. Among molecules associated with nucleosomal components, HMGB1, a non-histone protein, can emanate from activated and dying cells; HMGB1's immune activity is determined by post-translational modifications, redox state, and binding to other immune mediators. Although ANAs form complexes that deposit in the kidney or induce type 1 interferon, ANAs may also block immune activity. Together, these studies highlight the importance of complexes in the pathogenesis of lupus and their role as antigens, immunogens, and adjuvants.
Indexed as
Identifiers
What OpenQuestion holds
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.