Mechanisms of Transcriptional Regulation in Trisomy 21 and Their Contribution to Elevated Immune Signaling and Inflammation
DOI:
https://doi.org/10.33011/cuhj20265007Abstract
Down Syndrome, a condition caused by Trisomy 21 (T21), the triplication of human chromosome 21, leads to a variety of phenotypic manifestations that impact human health. Ranging from neurodegenerative diseases to autoimmune conditions, inflammation is a shared factor associated with these comorbidities: trisomic individuals experience heightened, chronic inflammation throughout their development and life. As a means to explore how transcriptional regulation differs between those with and without T21, pro-inflammatory cytokine interferon-gamma (IFNg) was used to perturb T21 and non-T21 cells, and nascent sequencing data was collected after 45 minutes. By comparing gene expression changes and broader activation of pathways, it was concluded that distinct genes separate the T21 and non-T21 response after IFNg perturbation, suggesting that transcriptional regulation may play a role in the distinctive inflammatory levels and comorbidities associated.
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11-August-2014
