English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Objective  Autoimmune Addison’s disease (AD) results from a combination of the genetic predisposition, unclear environmental triggers and ensuing immune dysfunction. MicroRNA molecules (miRNAs) are involved in post-transcriptional regulation of numerous target genes, hence may affect the immune function and promote autoimmunity. A deregulated miRNAs profile was reported in several autoimmune conditions. Our study was aimed at a global analysis of miRNA expression in CD4+ T cells from patients with AD.    Methods  CD4+ T cells were separated from peripheral blood, total RNA enriched in miRNAs extracted, and miRNA expression determined by small RNA sequencing. Global miRNA was investigated in 11 AD subjects and 9 age-matched healthy controls, with subsequent validation of the differentially expressed miRNAs by RT-qPCR in 29 patients and 28 controls.    Results  The analysis revealed upregulation of 9 miRNAs and downregulation of miR-509-3p in CD4+ T cells from patients with AD (cut-off fold change (FC) &gt;2, Benjamini–Hochberg  P   &lt; 0.05). RT-qPCR validation confirmed overexpression of miR-7977 ( P  &lt; 0.0001, FC = 2.7), miR-374a-5p and miR-1260b ( P  &lt; 0.05, FC = 1.3 and 1.2, respectively). miR-7977 was upregulated in patients with coexisting autoimmune conditions vs those with isolated AD ( P  = 0.005, mean FC = 2.2). Moreover, miR-7977 abundance appeared correlated with the number of autoimmune comorbidities ( P  &lt;0.0001, r = 0.736) and serum autoantibodies against thyroid peroxidase ( P  &lt; 0.001, r = 0.588).    Conclusions  Our study demonstrates upregulated expression of miR-7977 in CD4+ T cells from patients with AD, especially with its polyendocrine form. Further analyses are warranted to replicate our results, establish the marker utility of miR-7977, and elucidate its functional role in autoimmunity.

Overexpression of miR-7977 in CD4+ T cells is associated with multiplex autoimmunity in patients with Addison’s disease