ReviewCurrent opinion in immunology2025
Neuroimmune mechanisms of neuropsychiatric systemic lupus erythematosus.
Review in Current opinion 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.
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
4 citing papers in PubMed.
- Screening of diagnostic biomarkers for taurine metabolism-related genes in lupus nephritis and analysis of immune infiltration.International urology and nephrology · 2026Article
- Immunopathogenesis of neuropsychiatric systemic lupus erythematosus: current insights into inflammatory and thrombotic pathways.Journal of neuroinflammation · 2026Review
- Pathogenesis and therapeutic strategies for neuropsychiatric lupus centered on innate immune activation.Human cell · 2026Review
- Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
In systemic lupus erythematosus (SLE), chronic autoimmunity and sustained inflammation can lead to the development of neuropsychiatric lupus (NPSLE) in up to 80% of patients. Elevated interferon-alpha (IFNα) is detected in serum and cerebrospinal fluid, making it a major focus in studies investigating the mediators of NPSLE. Others have emphasized the role of autoantibodies, such as anti-dsDNA, which have been shown to cross-react with neurotransmitter receptors and directly damage neurons. In this review, we present an integrative framework in which immune complexes deposited in the neurovasculature trigger local IFNα production in the brain. We discuss how complement activation amplifies inflammation by recruiting monocytes and promoting transcriptional shifts in glial cells toward reactive and neurotoxic states. Together, cellular and soluble immune effectors converge to disrupt neuronal function and drive the behavioral symptoms characteristic of NPSLE.
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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.