ArticleGenetics and molecular biology2024
Expression profile of inflammasome genes in individuals with Down syndrome.
Article in Genetics and molecular biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.
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
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Who cites it
1 citing paper in PubMed, 1 synthesis or guideline pooled it.
- Revisiting down syndrome through the lens of interferonopathy and innate immune dysregulation.Frontiers in immunology · 2026Pooled it
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Down syndrome (DS), affecting 1 in 700 live births, is the most prevalent chromosomal disorder among newborns. Recognizable by classical clinical features, patients with DS are susceptible to various immunological misbalances. Inflammasome is (mis)activated in several immune-mediated diseases, however studies on individuals with DS are lacking. The present study evaluated the gene expression of NLRP1, NLRP3 and IL-1β in individuals with DS, aiming to understand their susceptibility to immune-mediated diseases. In addition, we assessed whether the individuals with DS present a differential inflammatory response after in vitro infection using PBMCs. For the gene expression assay, 20 individuals with DS and 15 healthy individuals for the control group (CT) were included, while the in vitro infection assay included 10 subjects. mRNA levels from individuals with DS group showed 1.9-fold change (FC) downregulation for NLRP1 (p=0.0001), but no differences for NLRP3 and IL1β. We did not observe significant differences between lipopolysaccharide (LPS)-treated and untreated cells in our in vitro assays. The differential expression of NLRP1 in individuals with DS suggests a potential association with susceptibility to the development of immune-mediated diseases, but further analysis is needed to confirm this relationship.
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Registered trials
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