ReviewClinical and experimental medicine2025
The role of DNASE1L3 in systemic lupus erythematosus: from pathogenesis to clinical implications.
Review in Clinical and experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
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
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Unraveling the Clinical Spectrum of DNASE1L3 Deficiency: Insights from Case Series and Systematic Literature Review.Current rheumatology reports · 2026Pooled it
- The SLC15A4-TASL complex is essential for lupus development in mice.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Immune response to DNA and RNA: structural insights, molecular mechanisms, and therapeutic targeting.Molecular biomedicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Systemic Lupus Erythematosus (SLE) is a chronic inflammatory autoimmune disease characterized by multi-organ damage, a complex interplay of immune dysregulation, and antibodies against nuclear macromolecules like DNA. Among these, anti-dsDNA antibodies are not only crucial diagnostic markers but also active participants in disease pathogenesis, forming immune complexes that deposit in various tissues and trigger inflammation. Emerging research has highlighted the critical role of Deoxyribonuclease 1-Like 3 (DNASE1L3), a secreted endonuclease, in maintaining homeostasis of cell-free DNA (cfDNA). Deficiencies or dysfunction of DNASE1L3, whether due to genetic mutations or neutralizing autoantibodies, lead to impaired clearance of cfDNA derived from apoptotic cells, microparticles, and Neutrophil Extracellular Traps (NETs). This accumulation of cfDNA plays an important role in SLE. This review explores the characteristics of DNASE1L3, the current status of research on the mechanisms through which its defects contribute to SLE pathogenesis, and its promising potential in the clinical diagnosis, monitoring, and treatment of this complex disease.
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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 Socratic graph.