ArticleBrain, behavior, and immunity2025
Sustained NPSLE-like phenotype in the absence of systemic lupus-like disease in TLR7-deficient B6.Nba2 mice.
Article in Brain, behavior, and immunity, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
2 citing papers in PubMed.
- Endothelial Dysfunction: Insights into Systemic Lupus Erythematosus-associated Cardiovascular Disease and Neuropsychiatric Manifestations.Journal of cardiovascular translational research · 2026Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
objectiveTo investigate the role of Toll-like Receptor 7 (TLR7) in the development of neuropsychiatric lupus (NPSLE) in the B6.Nba2 murine model of SLE.
methodsTLR7-deficient B6.Nba2 mice were evaluated for the development of NPSLE symptoms through behavioral testing with comparison groups of wild-type NPSLE-prone B6.Nba2 and B6 controls. Behavioral testing results were evaluated in the context of biomarker data, including flow cytometry for immune cell activation, and enzyme-linked immunosorbent assays (ELISA) to measure serum cytokine and autoantibody levels, including autoantibodies against double stranded DNA (dsDNA) and DWEYS peptide. Brain and spleen tissues waere harvested, and immuno histochemical studies and inflammatory gene activation obtained via qPCR were further analyzed to characterize immune system activation and SLE and NPSLE development in the mice.
resultsTLR7-deficient mice exhibited reduced signs of systemic SLE, including decreased splenomegaly, anti-dsDNA titers, and immune cell activation compared to wild-type mice. However, TLR7-deficient mice displayed a similar behavioral pattern to the NPSLE-prone B6.Nba2 mice, indicating NPSLE development was not influenced by TLR7. Knockout of TLR7 in B6.Nba2 mice also led to increased expression of TLR4 and TLR9, which suggests a possible role for these receptors in NPSLE pathogenesis.
conclusionWhile systemic lupus-like disease in the B6.Nba2 mouse model is dependent on TLR7, NPSLE development is not and may be influenced by TLR4 and TLR9 signaling. Thus, there may be separate mechanisms driving peripheral SLE compared to NPSLE with possible implications for pharmacologic management.
Indexed as
Identifiers
What OpenQuestion holds
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.