Observational studyJournal of immunology research2021
Elevated Expression of the Long Noncoding RNA MAFTRR in Patients with Hashimoto's Thyroiditis.
Observational study in Journal of immunology research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Multi-ancestry genome-wide association study in all of Us for primary open-angle glaucoma.Scientific reports · 2026Article
- Multi-Ancestry Genome-Wide Association Study in All of Us for Primary Open- Angle Glaucoma.Research square · 2025Article
- Identification of BTK as an immune-related biomarker for Hashimoto's thyroiditis by integrated bioinformatic analysis.BMC immunology · 2025Article
- Expression levels of interleukin-17 and interferon-γ in peripheral blood and relationship with thyroid function in patients with Hashimoto's thyroiditis.Frontiers in molecular biosciences · 2025Article
- Comprehensive Analysis of lncRNA Expression Profile and the Potential Role of ENST00000604491 in Graves' Disease.Journal of immunology research · 2022Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLong noncoding RNAs (lncRNAs) represent an important novel class of noncoding RNA molecule greater than 200 nucleotides that play a key role in the regulation of autoimmune diseases. Previous studies have demonstrated that MAFTRR (MAF transcriptional regulator RNA) regulated Th1 cells differentiation by inhibiting the expression of MAF in activated CD4
methodsThirty-eight HT patients and thirty-eight healthy controls were enrolled in the study. The proportion of Th1 cells and CD8
resultsWe found that the proportion of circulating Th1 cells and the transcript levels of IFNG were increased in peripheral blood of the HT patients. The transcript levels of MAFTRR were significantly increased in the HT patients and positively correlated with the percentage of Th1 cells and serum levels of antithyroglobulin antibody and antithyroperoxidase antibody. The transcript levels of MAF, a transcription factor that inhibits Th1 cells activity and IFN-
conclusionMAFTRR is significantly augmented in the HT patients and may contribute to the pathogenic role of the Th1 cells response in HT.
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