ReviewJournal of clinical immunology2024
Mendelian Causes of Autoimmunity: the Lupus Phenotype.
Review in Journal of clinical immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 18 citations in OpenAlex.
- NAP1 switches from an activator to a limiter of interferon induction by trapping TBK1 in condensates.Nature communications · 2026Article
- Expanding the clinical spectrum of DNASE1L3-associated monogenic lupus: A case series of 4 syrian pediatric cases.Medicine · 2026Article
- Exome sequencing enables molecular diagnosis in 10% of early-onset or familial systemic lupus erythematosus cases.EBioMedicine · 2026Article
- Immune ontogeny in childhood-onset systemic lupus erythematosus: effect of immune maturity on disease phenotype and therapeutic responses.Frontiers in immunology · 2026Review
- The emerging clinical relevance of cell-free DNA in lupus: from mechanistic insights to therapeutic opportunities.Frontiers in immunology · 2026Review
- Neutrophil Extracellular Traps in Systemic Lupus Erythematosus: Pathogenic Mechanisms, Crosstalk with Oxidative Stress, and Antioxidant Therapeutic Potential.Antioxidants (Basel, Switzerland) · 2025Review
- Characterisation and diagnostic model of monogenic lupus.Immunologic research · 2025Article
- Single-centre comparison of non-familial, familial and monogenic lupus.Rheumatology (Oxford, England) · 2025Article
- Radiation Exposure Induced Blood-Brain Barrier Injury via Mitochondria-Mediated Sterile Inflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Post translational Modifications and Protein-Protein Interactome of Endemic Pemphigus in El Bagre, Colombia: A New Variant Analysis.Dermatology practical & conceptual · 2025Article
- Enhanced TLR7-dependent production of type I interferon by pDCs underlies pandemic chilblains.The Journal of experimental medicine · 2025Article
- CAR-T cell therapy for juvenile-onset autoimmune diseases: a promising future?Arthritis research & therapy · 2025Review
- How (Ultra-)Rare Gene Variants Improve Our Understanding of More Common Autoimmune and Inflammatory Diseases.ACR open rheumatology · 2025Review
- Lupus Nephritis from Pathogenesis to New Therapies: An Update.International journal of molecular sciences · 2024Review
- Fish oil supplementation and risk of incident systemic lupus erythematosus: a large population-based prospective study.Nutrition journal · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that is characterized by its large heterogeneity in terms of clinical presentation and severity. The pathophysiology of SLE involves an aberrant autoimmune response against various tissues, an excess of apoptotic bodies, and an overproduction of type-I interferon. The genetic contribution to the disease is supported by studies of monozygotic twins, familial clustering, and genome-wide association studies (GWAS) that have identified numerous risk loci. In the early 70s, complement deficiencies led to the description of familial forms of SLE caused by a single gene defect. High-throughput sequencing has recently identified an increasing number of monogenic defects associated with lupus, shaping the concept of monogenic lupus and enhancing our insights into immune tolerance mechanisms. Monogenic lupus (moSLE) should be suspected in patients with either early-onset lupus or syndromic lupus, in male, or in familial cases of lupus. This review discusses the genetic basis of monogenic SLE and proposes its classification based on disrupted pathways. These pathways include defects in the clearance of apoptotic cells or immune complexes, interferonopathies, JAK-STATopathies, TLRopathies, and T and B cell dysregulations.
Indexed as
Identifiers
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.