Objective: Long non-coding RNAs (lncRNAs) comprise a large and diverse group of non-coding RNAs (ncRNAs) with important regulatory roles in various biological processes, including the immune system regulation. Rheumatoid arthritis (RA) as an autoimmune disease initiates inflammation in the synovial joints. T cells infiltrating into the synovial membrane have an important role in the pathogenesis of RA. The aim of the current investigation was to analyze the expression of four lncRNAs in the T cells from RA patients and healthy controls.
Methods: In the current study, we investigated the expression of GAS5, RMRP, IFNϒ-AS1, and THRIL lncRNAs in circulating T cells from 20 patients with RA and 18 healthy matched controls by quantitative real-time PCR. T cell isolation was accomplished using the MAC method. We also analyzed the correlation between lncRNA expression and clinical parameters. Also, the mRNA expression levels of IL-17 and TNF-α and the association between lncRNAs and these cytokines were examined.
Results: The results indicate that T cells of RA patients display increased levels of GAS5 (3.31-fold, p = 0.007), RMRP (2.43-fold, p = 0.02), and THRIL (2.14-fold, p = 0.03) lncRNAs compared with those of controls. Furthermore, a positive correlation was found between RMRP expression and disease duration in RA. Receiver operating characteristic (ROC) curve of GAS5, RMRP, and THRIL has a discriminative value in comparing RA patients and controls.
Conclusion: The results suggest lncRNAs may be involved in T cell dysfunction in RA. Further studies are required to see whether these lncRNAs have an effect on dysregulation of immune responses in RA disease. Key Points • 70% of non-coding sequences in the human genome are transcribed to RNA. • A growing body of evidence shows the importance of lncRNAs in innate and adaptive immune cell differentiation and functions. • Important recent works suggest a key role of immune cell lncRNAs in autoimmune processes and diseases including RA.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1007/s10067-019-04694-z | DOI Listing |
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!