ArticleFrontiers in immunology2019
Antiviral Adaptor MAVS Promotes Murine Lupus With a B Cell Autonomous Role.
Article 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 10 papers.
What it found
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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.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Immunopathogenesis and Therapeutics of Systemic Lupus Erythematosus: an Integrative Review.Clinical reviews in allergy & immunology · 2025Review
- CD11c-Cre driven deletion ofFrontiers in immunology · 2025Article
- Pathogenic cellular and molecular mediators in lupus nephritis.Nature reviews. Nephrology · 2023Review
- MAVS Positively Regulates Mitochondrial Integrity and Metabolic Fitness in B Cells.ImmunoHorizons · 2023Article
- Mitochondria in innate immunity signaling and its therapeutic implications in autoimmune diseases.Frontiers in immunology · 2023Review
- A Study on MDA5 Signaling in Splenic B Cells from an Imiquimod-Induced Lupus Mouse Model with Proteomics.Cells · 2022Article
- Application and prospect of targeting innate immune sensors in the treatment of autoimmune diseases.Cell & bioscience · 2022Review
- T Cell Homeostatic Proliferation Promotes a Redox State That Drives Metabolic and Epigenetic Upregulation of Inflammatory Pathways in Lupus.Antioxidants & redox signaling · 2022Review
- Women in immunology: 2020 and beyond.Nature immunology · 2020Review
- Innate Immune Sensing by Cells of the Adaptive Immune System.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Systemic lupus erythematosus (SLE) is an autoimmune disorder characterized by increased production of autoantibodies, which commonly target nuclear antigens, and concomitant deposition of immune complexes that cause inflammation in tissues. SLE is often associated with increased systemic expression of type I interferons, in some cases due to dysregulation in nucleic acid-sensing innate pathways. There is strong genetic evidence for a link between cytoplasmic RNA sensing pathways (RIG-I/MDA5) and SLE, both in human patients and murine models, however questions still remain regarding pathway initiation, cell types involved and downstream effects. Here we show that MAVS, an essential adaptor for RIG-I/MDA5 signaling, is necessary for all symptoms of autoimmune disease that develop spontaneously in the lupus model FcγRIIB
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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 OpenQuestion graph.