ReviewJournal of biomedicine & biotechnology2011
The MRL/lpr mouse strain as a model for neuropsychiatric systemic lupus erythematosus.
Review in Journal of biomedicine & biotechnology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed.
- PTGS2/COX-2 is associated with neurovascular and blood-brain barrier changes in behaviourally classified MRL/lpr mice.Lupus science & medicine · 2026Article
- Salmonella infection and biofilms drive anti-C1q and anti-dsDNA autoantibodies in systemic autoimmunity.PLoS pathogens · 2026Article
- Integrative Transcriptomic Analysis Reveals Impaired Oligodendrocyte Maturation and Myelination Signature in the Hippocampus of a Murine Model of Neuropsychiatric Lupus.International journal of molecular sciences · 2026Article
- Pathogenesis and therapeutic strategies for neuropsychiatric lupus centered on innate immune activation.Human cell · 2026Review
- IFNγ-associated immune-metabolic remodeling is linked to serotonin-kynurenine imbalance and cortical vulnerability in lupus-prone mice.Frontiers in immunology · 2026Article
- The pH-Dependent Specificity of Cathepsin S and Its Implications for Inflammatory Communications and Disease.Biochemistry · 2025Article
- Evaluating Neuropsychiatric Disease in Mouse Models of Systemic Lupus Erythematosus.Current protocols · 2025Article
- Blood-CSF barrier clearance of ABC transporter substrates is suppressed by interleukin-6 in lupus choroid plexus spheroids.Fluids and barriers of the CNS · 2025Article
- Changes in Gut Microbiota According to Disease Severity in a Lupus Mouse Model.International journal of molecular sciences · 2025Article
- The MRL Model: A Valuable Tool in Studies of Autoimmunity-Brain Interactions.Methods in molecular biology (Clifton, N.J.) · 2025Review
- Animal models of neuropsychiatric systemic lupus erythematosus: deciphering the complexity and guiding therapeutic development.Autoimmunity · 2024Review
- Article
- Deciphering Mechanisms, Prevention Strategies, Management Plans, Medications, and Research Techniques for Strokes in Systemic Lupus Erythematosus.Medicines (Basel, Switzerland) · 2024Review
- Constitutive knockout of interleukin-6 ameliorates memory deficits and entorhinal astrocytosis in the MRL/lpr mouse model of neuropsychiatric lupus.Journal of neuroinflammation · 2024Article
- Autoimmune and neuropsychiatric phenotypes in aFrontiers in immunology · 2024Article
- Article
- Treatment with lysophosphatidic acid prevents microglial activation and depression-like behaviours in a murine model of neuropsychiatric systemic lupus erythematosus.Clinical and experimental immunology · 2023Article
- Pristane induced lupus mice as a model for neuropsychiatric lupus (NPSLE).Behavioral and brain functions : BBF · 2023Article
- Mouse models, antibodies, and neuroimaging: Current knowledge and future perspectives in neuropsychiatric systemic lupus erythematosus (NPSLE).Frontiers in psychiatry · 2023Review
- Choroid Plexus-Infiltrating T Cells as Drivers of Murine Neuropsychiatric Lupus.Arthritis & rheumatology (Hoboken, N.J.) · 2022Article
1 more citing papers are in PubMed but not listed here.
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2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To date, CNS disease and neuropsychiatric symptoms of systemic lupus erythematosus (NP-SLE) have been understudied compared to end-organ failure and peripheral pathology. In this review, we focus on a specific mouse model of lupus and the ways in which this model reflects some of the most common manifestations and potential mechanisms of human NP-SLE. The mouse MRL lymphoproliferation strain (a.k.a. MRL/lpr) spontaneously develops the hallmark serological markers and peripheral pathologies typifying lupus in addition to displaying the cognitive and affective dysfunction characteristic of NP-SLE, which may be among the earliest symptoms of lupus. We suggest that although NP-SLE may share common mechanisms with peripheral organ pathology in lupus, especially in the latter stages of the disease, the immunologically privileged nature of the CNS indicates that early manifestations of particularly mood disorders maybe derived from some unique mechanisms. These include altered cytokine profiles that can activate astrocytes, microglia, and alter neuronal function before dysregulation of the blood-brain barrier and development of clinical autoantibody titres.
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