ReviewTranslational research : the journal of laboratory and clinical medicine2015
Interferon regulatory factors: critical mediators of human lupus.
Review in Translational research : the journal of laboratory and clinical medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 40 citations in OpenAlex.
- Contribution of localmBio · 2026Article
- The Type I Interferon Axis in Systemic Autoimmune Diseases: From Molecular Pathways to Targeted Therapy.Biomolecules · 2025Review
- The multiple roles of interferon regulatory factor family in health and disease.Signal transduction and targeted therapy · 2024Review
- Type I Interferons in Systemic Autoimmune Rheumatic Diseases: Pathogenesis, Clinical Features and Treatment Options.Mediterranean journal of rheumatology · 2024Review
- Exploring the shared mechanism of fatigue between systemic lupus erythematosus and myalgic encephalomyelitis/chronic fatigue syndrome: monocytic dysregulation and drug repurposing.Frontiers in immunology · 2024Article
- The Role of Genetic Risk Factors in Pathogenesis of Childhood-Onset Systemic Lupus Erythematosus.Current issues in molecular biology · 2023Review
- Type I Interferons in Autoimmunity.The Journal of investigative dermatology · 2022Review
- Altered function and differentiation of age-associated B cells contribute to the female bias in lupus mice.Nature communications · 2021Article
- Autosomal Recessive ISG15 Deficiency Underlies Type I Interferonopathy with Systemic Lupus Erythematosus and Inflammatory Myositis.Journal of clinical immunology · 2021Article
- Emerging roles of circular RNAs in systemic lupus erythematosus.Molecular therapy. Nucleic acids · 2021Review
- Leveraging Heterogeneity in Systemic Lupus Erythematosus for New Therapies.Trends in molecular medicine · 2021Review
- Type I Interferons in Systemic Autoimmune Diseases: Distinguishing Between Afferent and Efferent Functions for Precision Medicine and Individualized Treatment.Frontiers in pharmacology · 2021Review
- miR-106b-5p Inhibits IRF1/IFN-β Signaling to Promote M2 Macrophage Polarization of Glioblastoma.OncoTargets and therapy · 2020Article
- TheThe Indian journal of medical research · 2018Article
- Type I interferon in rheumatic diseases.Nature reviews. Rheumatology · 2018Review
- Updates in Lupus Genetics.Current rheumatology reports · 2017Review
- Review
- Absent in Melanoma 2 proteins in SLE.Clinical immunology (Orlando, Fla.) · 2017Review
- Effects of IRF1 and IFN-β interaction on the M1 polarization of macrophages and its antitumor function.International journal of molecular medicine · 2016Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The pathogenesis of systemic lupus erythematosus (SLE) is multifactorial, and the interferon regulatory factors (IRFs) play an important role. Autoantibodies formed in SLE target nuclear antigens, and immune complexes formed by these antibodies contain nucleic acid. These immune complexes can activate antiviral pattern recognition receptors (PRRs), resulting in the downstream activation of IRFs, which can induce type I interferon (IFN-I) and other inflammatory mediators. Genetic variations in IRFs have been associated with susceptibility to SLE, and current evidence supports the idea that these polymorphisms are gain of function in humans. Recent studies suggest that these genetic variations contribute to the break in humoral tolerance that allows for nucleic acid binding autoantibodies, and that the same polymorphisms also augment IFN-I production in the presence of these autoantibody immune complexes, forming a feed-forward loop. In this review, we will outline major features of the PRR/IRF systems and describe the role of the IRFs in human SLE pathogenesis.
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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.