Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (599 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A chronic, relapsing, inflammatory, and often febrile multisystemic disorder of connective tissue, characterized principally by involvement of the skin, joints, kidneys, and serosal membranes. It is of unknown etiology, but is thought to represent a failure of the regulatory mechanisms of the autoimmune system. The disease is marked by a wide range of system dysfunctions, an elevated erythrocyte sedimentation rate, and the formation of LE cells in the blood or bone marrow.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Lupus Erythematosus Disseminatus; Systemic Lupus Erythematosus; Libman-Sacks Disease; Disease, Libman-Sacks; Libman Sacks Disease.
Where it fits in the MeSH classification
- Broader topics
- Connective Tissue Diseases; Autoimmune Diseases
- Narrower topics
- Lupus Nephritis; Lupus Vasculitis, Central Nervous System
- See also
- Lupus Coagulation Inhibitor; Antiphospholipid Syndrome; Vasculitis, Central Nervous System
Research landscape
PubMed indexes 73,909 records tagged with the MeSH heading “Lupus Erythematosus, Systemic” (counts retrieved 2026-10-29). 14,389 of them (19.5%) were published from 2020 onward, and the busiest period so far is through 1999 with 29,015 records.
Reviews account for 11,988 records (16.2%) and meta-analyses for 890. Randomized controlled trials number 718 (1.0%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 29,015 |
| 2000-2009 | 13,050 |
| 2010-2019 | 17,455 |
| 2020 onward | 14,389 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 11,988 | 16.2% |
| Meta-analyses | 890 | 1.2% |
| Randomized controlled trials | 718 | 1.0% |
Method: PubMed query "Lupus Erythematosus, Systemic"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in immunology
Immune responses are studied in model organisms, in cells from donors and in patients, and the same pathway can behave differently across these settings. Mouse immune systems differ from human ones in important ways, and blood measurements may not reflect what happens in tissues. Clinical conclusions about immune-mediated disease or immunotherapy come mainly from controlled trials and long-term cohorts. Check the species and tissue studied, whether markers were linked to outcomes patients notice, and the follow-up time.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Applications of artificial intelligence in systemic lupus erythematosus: integrating multi-omics data for precision medicine | 2026 | Review article Design not recorded in structured metadata | 3 | cc by PMID 42183196 · DOI · PMC13189759 |
| Efficacy and safety of telitacicept in systemic lupus erythematosus: a single-center, retrospective, real-world study | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42582193 · DOI · PMC13457300 |
| Mitochondrial DNA in systemic lupus erythematosus: pathogenic mechanisms, clinical biomarkers, and precision therapeutic strategies | 2026 | Review article Design not recorded in structured metadata | 1 | cc by PMID 42662156 · DOI · PMC13519981 |
Applications of artificial intelligence in systemic lupus erythematosus: integrating multi-omics data for precision medicine [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Systemic lupus erythematosus (SLE) is a clinically and biologically heterogeneous autoimmune disease in which patients with similar or disparate clinical phenotypes can exhibit distinct molecular drivers.
- Closing excerpt
- If key barriers to clinical translation can be overcome, AI-based methods hold promise for achieving truly personalized approaches in the management of SLE.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (253 words)
Systemic lupus erythematosus (SLE) is a clinically and biologically heterogeneous autoimmune disease in which patients with similar or disparate clinical phenotypes can exhibit distinct molecular drivers. This heterogeneity limits the utility of traditional, largely linear, analytic approaches and contributes to variations in diagnosis, prognosis, and therapeutic outcome. Artificial intelligence (AI), including machine learning (ML) and deep learning (DL), offers a complementary framework for extracting nonlinear patterns from complex biomedical datasets and for translating high dimensional molecular measurements into actionable clinical signatures. Here, we review how supervised and unsupervised ML methods are being applied to SLE, with a focus on multi-omics integration across genomics, transcriptomics, proteomics, and metabolomics. In this review, we specifically focus on how these approaches can define molecular endotypes, explaining heterogeneity in disease course and therapeutic response. We summarize evidence that AI-driven endotyping can reproducibly separate patients into molecularly defined subgroups dominated by distinct immune signatures and facilitate biomarker discovery and improved risk modelling. We highlight the limitations of conventional clinical phenotyping and the need for AI-driven biologically grounded patient stratification. Importantly, we frame these advances within a systems biology perspective, in which AI-driven integration of multi-omics and clinical data enables a unified approach to disease diagnosis, molecular stratification, prognosis, and therapeutic response prediction in SLE. Despite these advances, most AI-derived predictors remain research-grade, and require prospective multi-center validation and explicit demonstration of clinical utility before routine deployment. If key barriers to clinical translation can be overcome, AI-based methods hold promise for achieving truly personalized approaches in the management of SLE.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42183196 · DOI · PMC13189759
Efficacy and safety of telitacicept in systemic lupus erythematosus: a single-center, retrospective, real-world study [2]
Abstract reading summary — source excerpts
- Opening excerpt
- ObjectiveTo explore the real-world efficacy and safety of telitacicept in patients with systemic lupus erythematosus (SLE).
- Closing excerpt
- 58 at 12, 24, and 52 weeks, respectively (P P P P P ConclusionIn this real-world study, telitacicept combined with conventional therapy was associated with improvements in disease activity and organ functions in SLE with favorable safety.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (125 words)
ObjectiveTo explore the real-world efficacy and safety of telitacicept in patients with systemic lupus erythematosus (SLE).MethodsThis retrospective study included SLE patients treated with telitacicept for at least 3 months at Mianyang Central Hospital between January 2022 and December 2025. Baseline characteristics and clinical outcomes at 12, 24, and 52 weeks were assessed.ResultsA total of 139 patients were enrolled in this study. The SLE Disease Activity Index 2000 (SLEDAI-2K) score significantly decreased from a baseline of 11.42 ± 4.68 to 4.623 ± 3.65, 2.42 ± 2.98, and 1.48 ± 2.58 at 12, 24, and 52 weeks, respectively (P P P P P ConclusionIn this real-world study, telitacicept combined with conventional therapy was associated with improvements in disease activity and organ functions in SLE with favorable safety.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42582193 · DOI · PMC13457300
Mitochondrial DNA in systemic lupus erythematosus: pathogenic mechanisms, clinical biomarkers, and precision therapeutic strategies [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Mitochondrial DNA (mtDNA) is increasingly recognized as an active driver of immune dysregulation in systemic lupus erythematosus (SLE), yet most existing reviews treat it as a single damage signal rather than a multifunctional pathological mediator.
- Closing excerpt
- Incorporating mtDNA-based biomarkers into clinical monitoring and developing precision strategies targeting mtDNA-driven inflammatory circuits represent important steps toward individualized SLE management.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (221 words)
Mitochondrial DNA (mtDNA) is increasingly recognized as an active driver of immune dysregulation in systemic lupus erythematosus (SLE), yet most existing reviews treat it as a single damage signal rather than a multifunctional pathological mediator. This review presents an integrated framework examining mtDNA as a central hub linking mitochondrial dysfunction to systemic autoimmunity. We conducted a comprehensive synthesis of published evidence on mtDNA biology, its dysregulation in SLE, organ-specific injury mechanisms, and the clinical landscape of mtDNA-targeted therapeutic strategies. In SLE, intracellular mtDNA depletion coexists paradoxically with markedly elevated circulating cell-free mtDNA, a pattern correlating with disease activity and organ involvement. Sequential cytoplasmic and extracellular release of mtDNA engages cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING), Toll-like receptor 9 (TLR9), and inflammasome platforms, establishing self-amplifying interferon and pro-inflammatory circuits that drive multi-organ pathology. We consolidate emerging evidence for mtDNA-related parameters as clinical biomarkers and propose a provisional patient stratification framework distinguishing two pathological subtypes with distinct therapeutic implications. Among current therapeutic strategies, N-acetylcysteine (NAC) and metformin carry the strongest clinical evidence, while cGAS-STING inhibitors and TLR9 antagonists represent compelling emerging candidates. mtDNA operates as an integrative pathological hub in SLE, and its dysregulation pattern carries both diagnostic and therapeutic significance. Incorporating mtDNA-based biomarkers into clinical monitoring and developing precision strategies targeting mtDNA-driven inflammatory circuits represent important steps toward individualized SLE management.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42662156 · DOI · PMC13519981
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Global epidemiology of systemic lupus erythematosus: a comprehensive systematic analysis and modelling study [4]
- Research article Prevalence of Systemic Lupus Erythematosus in the United States: Estimates From a Meta-Analysis of the Centers for Disease Control and Prevention National Lupus Registries [5]
- Research article Meta-analysis of 208370 East Asians identifies 113 susceptibility loci for systemic lupus erythematosus [6]
- Research article Gut dysbiosis in rheumatic diseases: A systematic review and meta-analysis of 92 observational studies [7]
- Research article Prevalence and metric of depression and anxiety in systemic lupus erythematosus: A systematic review and meta-analysis [8]
- Research article Vitamin D status in patients with systemic lupus erythematosus (SLE): A systematic review and meta-analysis [9]
References
- Biswas B, Munquad S, Roy Choudhury K, Cherayil BJ, Chaudhuri A. Applications of artificial intelligence in systemic lupus erythematosus: integrating multi-omics data for precision medicine. . 2026. PMID 42183196 · DOI · PMC13189759
- Yang L, Liu J, Zou J, Yang J. Efficacy and safety of telitacicept in systemic lupus erythematosus: a single-center, retrospective, real-world study. . 2026. PMID 42582193 · DOI · PMC13457300
- Huang F, Sun K, Diao L, Lu K, Fan Y, Xie G. Mitochondrial DNA in systemic lupus erythematosus: pathogenic mechanisms, clinical biomarkers, and precision therapeutic strategies. . 2026. PMID 42662156 · DOI · PMC13519981
- Tian J, Zhang D, Yao X, Huang Y, Lu Q. Global epidemiology of systemic lupus erythematosus: a comprehensive systematic analysis and modelling study. Ann Rheum Dis. 2023. PMID 36241363 · DOI · PMC9933169
- Izmirly PM, Parton H, Wang L, McCune WJ, Lim SS, Drenkard C, et al.. Prevalence of Systemic Lupus Erythematosus in the United States: Estimates From a Meta-Analysis of the Centers for Disease Control and Prevention National Lupus Registries. Arthritis Rheumatol. 2021. PMID 33474834 · DOI · PMC8169527
- Yin X, Kim K, Suetsugu H, Bang SY, Wen L, Koido M, et al.. Meta-analysis of 208370 East Asians identifies 113 susceptibility loci for systemic lupus erythematosus. Ann Rheum Dis. 2021. PMID 33272962 · DOI · PMC8053352
- Wang Y, Wei J, Zhang W, Doherty M, Zhang Y, Xie H, et al.. Gut dysbiosis in rheumatic diseases: A systematic review and meta-analysis of 92 observational studies. EBioMedicine. 2022. PMID 35594658 · DOI · PMC9120231
- Moustafa AT, Moazzami M, Engel L, Bangert E, Hassanein M, Marzouk S, et al.. Prevalence and metric of depression and anxiety in systemic lupus erythematosus: A systematic review and meta-analysis. Semin Arthritis Rheum. 2020. PMID 31303437 · DOI
- Islam MA, Khandker SS, Alam SS, Kotyla P, Hassan R. Vitamin D status in patients with systemic lupus erythematosus (SLE): A systematic review and meta-analysis. Autoimmun Rev. 2019. PMID 31520805 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.