ReviewF1000Research2019
The central role of nucleic acids in the pathogenesis of systemic lupus erythematosus.
Review in F1000Research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 28 citations in OpenAlex.
- Anti-ribosomal-P protein antibodies and systemic lupus erythematosus (SLE): in a cross-sectional study of Danish adult patients with SLE, no significant association is found between anti-ribosomal-P and neuropsychiatric SLE.Lupus science & medicine · 2025Article
- A lupus-derived autoantibody that binds to intracellular RNA activates cGAS-mediated tumor immunity and can deliver RNA into cells.Science signaling · 2025Article
- Adjunctive molecular hydrogen therapy for refractory malar rash in systemic lupus erythematosus: A case report with immunological insights.SAGE open medical case reports · 2025Article
- Unique Interplay Between Antinuclear Antibodies and Nuclear Molecules in the Pathogenesis of Systemic Lupus Erythematosus.Arthritis & rheumatology (Hoboken, N.J.) · 2024Review
- The role of DNA in the pathogenesis of SLE: DNA as a molecular chameleon.Annals of the rheumatic diseases · 2024Review
- Moonlighting chromatin: when DNA escapes nuclear control.Cell death and differentiation · 2023Review
- Anti-DNA-IgM Favors the Detection of NET-Associated Extracellular DNA.International journal of molecular sciences · 2023Article
- Recombinant Klotho attenuates IFNγ receptor signaling and SAMHD1 expression through blocking NF-κB translocation in glomerular mesangial cells.International journal of medical sciences · 2023Article
- Heterogeneity of antibody-secreting cells infiltrating autoimmune tissues.Frontiers in immunology · 2023Review
- Amyloid-containing biofilms and autoimmunity.Current opinion in structural biology · 2022Review
- The interaction of anti-DNA antibodies with DNA antigen: Evidence for hysteresis for high avidity binding.Clinical immunology (Orlando, Fla.) · 2021Article
- Review
- Camptothecin and Topotecan, Inhibitors of Transcription Factor Fli-1 and Topoisomerase, Markedly Ameliorate Lupus Nephritis in (NZB × NZW)F1 Mice and Reduce the Production of Inflammatory Mediators in Human Renal Cells.Arthritis & rheumatology (Hoboken, N.J.) · 2021Article
- DNA-nanoparticle interactions: Formation of a DNA corona and its effects on a protein corona.Biointerphases · 2020Article
- The basic and translational science year in review: Confucius in the era of Big Data.Seminars in arthritis and rheumatism · 2020Review
- Article
- Circular RNAs and RNase L in PKR activation and virus infection.Cell & bioscience · 2019Article
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 whose pathogenesis can be conceptualized by a model based on a central role for immune complexes (ICs) between antinuclear antibodies and nucleic acids. According to this model, ICs can promote pathogenesis by two main mechanisms: deposition in the tissue to incite local inflammation and interaction with cells of the innate immune system to stimulate the production of cytokines, most prominently type 1 interferon. The latter stimulation results from the uptake of DNA and RNA in the form of ICs into cells and subsequent signaling by internal nucleic acid sensors for DNA and RNA. These sensors are likely important for the response to intracellular infection, although they may also be triggered during cell stress or injury by DNA or RNA aberrantly present in the cytoplasm. For IC formation, a source of extracellular DNA and RNA is essential. The current model of SLE posits that cell death is the origin of the nucleic acids in the ICs and that impairment of clearance mechanisms increases the amount of nuclear material in the extracellular space. This model of SLE is important since it points to new approaches to therapy; agents targeting interferon or the interferon receptor are examples of therapeutic approaches derived from this model. Future studies will explore novel biomarkers to monitor the operation of these mechanisms and to elucidate other steps in pathogenesis that can be targeted for therapy.
Indexed as
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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.