ReviewFrontiers in immunology2025
Myeloid cells as IFNα producers in systemic lupus erythematosus.
Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
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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
4 citing papers in PubMed.
- Targeting FOXP3 and Regulatory T Cells in Systemic Lupus Erythematosus: Emerging Therapeutic Strategies and Clinical Prospects.Journal of cellular biochemistry · 2026Review
- Intestinal and Blood-Brain Barrier Dysfunction in Lupus: Emerging Mechanisms and Modulation by Cinnamon.Molecules (Basel, Switzerland) · 2026Review
- Gene expression profiling of dendritic cell tolerance dysfunction in women with systemic lupus erythematosus.Frontiers in immunology · 2026Article
- Escape From X Chromosome Inactivation as a Driver of Plasmacytoid DC Heterogeneity in Health and Disease.Immunological reviews · 2025Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type I interferons (IFNs) play crucial roles in the pathogenesis of systemic lupus erythematosus (SLE). Plasmacytoid dendritic cells (pDCs) stimulated by Toll-like receptor (TLR) pathways have been thought to be the major producers of IFNα in patients with SLE. However, the responsiveness of pDCs from SLE patients to stimuli that produce IFNα differs depending on the type of TLR pathway involved. In addition to pDCs, monocytes from SLE patients were found to produce IFNα when responding to the cGAS-STING pathway. Here, we outline the major pathways that induce IFNα production by myeloid cells in SLE, and the possible mechanisms by which IFNα overproduction occurs by these cells. Finally, we discuss the current and future therapeutic strategies to regulate IFNα production in patients with SLE.
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Registered trials
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