ArticleAnimal models and experimental medicine2026
Phenotypic profiling of pristane-induced mimicking human systemic lupus erythematosus in Macaca fascicularis.
Article in Animal models and experimental medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe development of nonhuman primate models that replicate human systemic lupus erythematosus (SLE) remains limited. This study aimed to develop a pristane-induced SLE model in Macaca fascicularis and evaluate its capacity to mimic human-like clinical and laboratory immunological alterations.
methodsAn experimental, single-arm investigation was performed using six female M. fascicularis (2-3 years old, 3-4 kg), which received a single intraperitoneal pristane injection (5 mL/kg body weight) to induce SLE and were monitored biweekly.
resultsThroughout the 24-week study period, all macaques developed hallmark SLE-like changes without requiring a booster, including a pronounced increase in antinuclear antibody titers (p = 0.002), with anti-dsDNA positivity detected at the study endpoint. Significant decline was observed in hemoglobin, leukocyte, and lymphocyte count (p < 0.05), reflecting hematologic perturbations consistent with human SLE. Physiologic deterioration, manifested as hyperthermia and weight loss, also emerged early (p = 0.001). Biochemical assessment demonstrated mild hepatic and renal dysfunction marked by elevated serum glutamic pyruvic transaminase (SGPT) and urea concentrations (p < 0.05). Uniform proteinuria further indicated renal involvement, although the absence of hematuria suggests a spectrum of renal injury that may be less severe than that observed in advanced human SLE and may require longer observation.
conclusionOverall, the reproducibility of autoantibody elevation and multisystem involvement demonstrates the model's translational potential. This nonhuman primate model offers a significant framework for investigating SLE pathogenesis and assessing novel therapy approaches.
Indexed as
Identifiers
What Socratic 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 Socratic graph.