ArticleAnimal models and experimental medicine2025
The NLRP3 inflammasome pathway contributes to chronic inflammation in experimental autoimmune uveitis.
Article in Animal models and experimental medicine, 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.
- Type III interferons attenuates Th1/Th17 cell pathogenicity and regulates retinal pigment epithelium cells via NLRP1/NLRP3 signaling axis in autoimmune uveitis.Genes & diseases · 2026Article
- The NLRP3 inflammasome pathway contributes to chronic inflammation in experimental autoimmune uveitis.Animal models and experimental medicine · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
backgroundNoninfectious uveitis, a chronic ocular inflammatory disease, is characterized by the activation of immune cells in the eye, with most studies focusing on the role of the adaptive immune system in the disease. However, limited data exist on the potential contribution of the innate immune system, specifically the nucleotide-binding oligomerization domain and leucine-rich repeat receptor-3 (NLRP3) inflammasome pathway. This pathway has previously been identified as a driver of inflammation in several low-grade, progressive inflammatory eye diseases such as diabetic retinopathy. The aim of this study was to determine whether the NLRP3 inflammasome pathway plays a role in the pathogenesis and chronicity of experimental autoimmune uveitis (EAU).
methodsEAU was induced in C57BL/6J mice via intraperitoneal pertussis toxin and subcutaneous interphotoreceptor retinoid-binding protein injections. After 12 weeks, eyes were enucleated, and whole eye sections were assessed for inflammasome, macrophage, and microglial markers in the retina, ciliary body, and cornea using immunohistochemistry.
resultsOur study confirmed higher NLRP3 inflammasome activation (increased expression of NLRP3 and cleaved caspase 1 labeling) in EAU mouse retinas compared to controls. This correlated with increased astrogliosis and microglial activation throughout the eye. Migratory innate and adaptive peripheral immune cells (macrophages and leukocytes) were also found within the retina and ciliary body of EAU mice. Connexin43 proteins, which form hexameric hemichannels that can release adenosine triphosphate (ATP), an upstream inflammasome priming signal, were also found upregulated in the retina and cornea of EAU mice.
conclusionOverall, our findings support the idea that in the EAU model there is active inflammation, even 12 weeks post induction, and that it can be correlated to inflammasome activation. This contributes to the pathogenesis and chronicity of noninfectious uveitis, and our results emphasize that targeting the inflammasome pathway could be efficacious for noninfectious uveitis treatment.
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.