ReviewFrontiers in immunology2019
Sources of Pathogenic Nucleic Acids in Systemic Lupus Erythematosus.
Review in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 70 citations in OpenAlex.
- Evaluation of RNase therapy in systemic lupus erythematosus: a randomised phase 2a clinical trial of RSLV-132.Lupus science & medicine · 2024Trial
- The therapeutic potential of transposable element activity modulation.EMBO molecular medicine · 2026Review
- Decoding Lupus Diagnosis, Pathogenesis and Therapy: From Systemic Autoimmunity to Renal Damage.Diagnostics (Basel, Switzerland) · 2026Review
- Belimumab in Systemic Lupus Erythematosus: From B-Cell Biology to Disease Modification.Journal of clinical medicine · 2026Review
- Article
- Pain in systemic lupus erythematosus: emerging insights and paradigms.Nature reviews. Rheumatology · 2025Review
- Article
- A lupus-derived autoantibody that binds to intracellular RNA activates cGAS-mediated tumor immunity and can deliver RNA into cells.Science signaling · 2025Article
- Association of hyperactivated transposon expression with exacerbated immune activation in systemic lupus erythematosus.Mobile DNA · 2024Article
- Subcellular location of L1 retrotransposon-encoded ORF1p, reverse transcription products, and DNA sensors in lupus granulocytes.Mobile DNA · 2024Article
- Anti-Toxoplasma gondii antibodies as a risk factor for the prevalence and severity of systemic lupus erythematosus.Parasites & vectors · 2024Article
- Pathogenic cellular and molecular mediators in lupus nephritis.Nature reviews. Nephrology · 2023Review
- Interaction between Long Noncoding RNAs and Syncytin-1/Syncytin-2 Genes and Transcripts: How Noncoding RNAs May Affect Pregnancy in Patients with Systemic Lupus Erythematosus.International journal of molecular sciences · 2023Article
- Phenotypic and functional characteristics of murine CD11c+ B cells which is suppressed by metformin.Frontiers in immunology · 2023Article
- Multiple RNA-binding proteins associated with long interspersed element-1 encoded ORF1p are targeted by the autoimmune response in systemic lupus erythematosus.Journal of cellular and molecular immunology · 2023Article
- Hyperresponsive cytosolic DNA-sensing pathway in monocytes from primary Sjögren's syndrome.Rheumatology (Oxford, England) · 2022Article
- The DNA sensors AIM2 and IFI16 are SLE autoantigens that bind neutrophil extracellular traps.eLife · 2022Article
- DNA damage contributes to neurotoxic inflammation in Aicardi-Goutières syndrome astrocytes.The Journal of experimental medicine · 2022Article
- Dysregulation and chronicity of pathogenic T cell responses in the pre-diseased stage of lupus.Frontiers in immunology · 2022Review
- Dysregulation of the cGAS-STING Pathway in Monogenic Autoinflammation and Lupus.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
A hallmark of systemic lupus erythematosus (SLE), and several related autoimmune diseases, is the presence of autoantibodies against nucleic acids and nucleic acid-binding proteins, as well as elevated type I interferons (IFNs), which appear to be instrumental in disease pathogenesis. Here we discuss the sources and proposed mechanisms by which a range of cellular RNA and DNA species can become pathogenic and trigger the nucleic acid sensors that drive type I interferon production. Potentially SLE-promoting DNA may originate from pieces of chromatin, from mitochondria, or from reverse-transcribed cellular RNA, while pathogenic RNA may arise from mis-localized, mis-processed, ancient retroviral, or transposable element-derived transcripts. These nucleic acids may leak out from dying cells to be internalized and reacted to by immune cells or they may be generated and remain to be sensed intracellularly in immune or non-immune cells. The presence of aberrant DNA or RNA is normally counteracted by effective counter-mechanisms, the loss of which result in a serious type I IFN-driven disease called Aicardi-Goutières Syndrome. However, in SLE it remains unclear which mechanisms are most critical in precipitating disease: aberrant RNA or DNA, overly sensitive sensor mechanisms, or faulty counter-acting defenses. We propose that the clinical heterogeneity of SLE may be reflected, in part, by heterogeneity in which pathogenic nucleic acid molecules are present and which sensors and pathways they trigger in individual patients. Elucidation of these events may result in the recognition of distinct "endotypes" of SLE, each with its distinct therapeutic choices.
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