ArticleJournal of translational autoimmunity2020
Inflammatory monocyte-derived dendritic cells mediate autoimmunity in murine model of systemic lupus erythematosus.
Article in Journal of translational autoimmunity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 11 citations in OpenAlex.
- Cutaneous Dendritic Cells: Structure, Function and Immune Role.Biomedicines · 2026Review
- NLRP12 is an innate immune checkpoint for repressing IFN signatures and attenuating lupus nephritis progression.The Journal of clinical investigation · 2023Article
- B cell-activating factor (BAFF) from dendritic cells, monocytes and neutrophils is required for B cell maturation and autoantibody production in SLE-like autoimmune disease.Frontiers in immunology · 2023Article
- Pathogenesis of Paradoxical Reactions Associated with Targeted Biologic Agents for Inflammatory Skin Diseases.Biomedicines · 2022Review
- Clinical outcomes of COVID-19 patients with rheumatic diseases: a retrospective cohort study and synthesis analysis in Wuhan, China.Clinical rheumatology · 2022Article
- Abnormal Changes of Monocyte Subsets in Patients With Sjögren's Syndrome.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Using a mouse model of systemic lupus erythematosus (SLE), we recently demonstrated that the two major manifestations of SLE are mechanistically independent because the type I IFN pathway leads to the autoantibody production whereas the NF-κB activation is sufficient for the development of glomerulonephritis. To further advance our understandings on the molecular pathways regulating the development of SLE, we studied the role of IRF8 because it controls both type I IFN and NF-κB pathways and saw that IRF8-deficient mice failed to develop either glomerulonephritis or the autoantibody production. Furthermore, these genetically engineered mice prompted us to realize the important role of Ly6C
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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.