ArticleJournal of autoimmunity2013
Anti-DNA antibodies cross-react with C1q.
Article in Journal of autoimmunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 39 citations in OpenAlex.
- Sera of Healthy First-Degree Relatives of SLE Patients Contain Autoantibodies to Globular Domains of C1q.Antibodies (Basel, Switzerland) · 2026Article
- C1q Is Recognized as a Soluble Autoantigen by Anti-C1q Antibodies of Patients with Systemic Lupus Erythematosus.Antibodies (Basel, Switzerland) · 2025Article
- Anti-C1q Autoantibody-Binding Engineered scFv C1q-Mimicking Fragment Enhances Disease Progression in Lupus-Prone MRL/lpr Mice.International journal of molecular sciences · 2025Article
- Philosophical and distinct SLE epitomes: dogmas in conflict with evidences and an intellectual dissonance between established pathophysiological models.Frontiers in immunology · 2025Review
- Precise Targeting of Autoantigen-Specific B Cells in Lupus Nephritis with Chimeric Autoantibody Receptor T Cells.International journal of molecular sciences · 2024Article
- 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
- Proteomic analyses reveal cystatin c is a promising biomarker for evaluation of systemic lupus erythematosus.Clinical proteomics · 2023Article
- Decipher the Immunopathological Mechanisms and Set Up Potential Therapeutic Strategies for Patients with Lupus Nephritis.International journal of molecular sciences · 2023Review
- Understanding the contextual functions of C1q and LAIR-1 and their applications.Experimental & molecular medicine · 2022Review
- Anti-Idiotype scFv Localizes an Autoepitope in the Globular Domain of C1q.International journal of molecular sciences · 2021Article
- Complement Deficiencies Result in Surrogate Pathways of Complement Activation in Novel Polygenic Lupus-like Models of Kidney Injury.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Autoimmunity and SLE: Factual and Semantic Evidence-Based Critical Analyses of Definitions, Etiology, and Pathogenesis.Frontiers in immunology · 2020Review
- ALW peptide ameliorates lupus nephritis in MRL/lpr mice.Arthritis research & therapy · 2019Article
- Anti-double Stranded DNA Antibodies: Origin, Pathogenicity, and Targeted Therapies.Frontiers in immunology · 2019Review
- 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
- Investigation of C1-complex regions reveals new C1Q variants associated with protection from systemic lupus erythematosus, and affect its transcript abundance.Scientific reports · 2018Article
- Amending HIV Drugs: A Novel Small-Molecule Approach To Target Lupus Anti-DNA Antibodies.Journal of medicinal chemistry · 2016Article
- Anti-C1q in systemic lupus erythematosus.Lupus · 2016Article
- SLE-associated risk factors affect DC function.Immunological reviews · 2016Review
- Immune mediators in the brain and peripheral tissues in autism spectrum disorder.Nature reviews. Neuroscience · 2015Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Systemic lupus erythematosus (SLE) is an autoimmune disorder that involves multiple organ systems and typically presents as a chronic inflammatory disease. Antibodies to double-stranded (ds) DNA are present in approximately 70% of patients and form nucleic acid containing immune complexes which activate dendritic cells through engagement of toll-like receptors, leading to a pro-inflammatory, pro-immunogenic milieu. In addition, anti-dsDNA antibodies deposit in kidneys to initiate glomerulonephritis. Antibodies to C1q have also been implicated in lupus nephritis and are found in 30-50% of patients. C1q is a known suppressor of immune activation and C1q deficiency is the strongest risk factor for SLE. We previously identified a subset of anti-DNA antibodies that binds the N-methyl-D-aspartate receptor. We now show that both mouse and human anti-DNA antibodies with this specificity bind C1q. These antibodies bind to Clq in glomeruli and exhibit decreased glomerular deposition in the absence of C1q. We propose that this subset of anti-DNA antibodies participates in lupus pathogenesis through direct targeting of C1q on glomeruli and also through removal of soluble C1q thereby limiting the ability of C1q to mediate immune homeostasis.
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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.