Life sciences · 2022
LncRNA MEG3 regulates the interplay between Th17 and Treg cells in Behçet's disease and systemic lupus erythematosus.
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Mehana Noha A, Ghaiad Heba R, Hassan Mariam, Elsabagh Yumn A, Labib Safa, Abd-Elmawla Mai A
Аннотация
BACKGROUND: Behçet's disease (BD) and systemic lupus erythematosus (SLE) are two autoimmune inflammatory diseases of indefinite etiology. However, up till now, no study has explored the exact regulatory mechanisms of lncRNA maternally expressed gene-3 (MEG3) over the balance between regulatory T-cells (Treg) and T helper-17 (Th17) cells in BD and SLE.
AIM: The current study aimed to investigate the role of lncRNA MEG3 in the interplay between the anti-inflammatory Treg/transcription factor forkhead box P3 (FOXP3) axis versus the pro-inflammatory Th17/retinoic acid orphan receptor-γt (RORγt) axis.
MAIN METHODS: 100 subjects, 35 with BD and 35 with SLE in addition to 30 healthy participants were included in the study. Gene expression analysis was performed and ShinyGO database was utilized for in-depth analysis and graphical visualization of the gene ontology (GO) and pathway enrichment analysis for lncRNA and the other target genes.
KEY FINDINGS: The current results demonstrate the upregulation of lncRNA MEG3 in BD but not SLE patients. Moreover, significant differences in RORγt and FOXP3 were found between BD and SLE patients. The present findings linked lncRNA MEG3 to BD activity scores as well as CRP levels. Finally, lncRNA MEG3 showed excellent diagnostic power for BD, in addition to adequate discriminative power that can be used to differentiate between BD and SLE.
SIGNIFICANCE: The current study objectively elucidated a framework for the involvement of Treg/Th17 through transcription factors RORγt and FOXP3, in addition to their links to the downstream cytokines network including TGF-ꞵ, IL-10, IL-17 and IL-23 in BD and SLE pathogenesis and activity.
AIM: The current study aimed to investigate the role of lncRNA MEG3 in the interplay between the anti-inflammatory Treg/transcription factor forkhead box P3 (FOXP3) axis versus the pro-inflammatory Th17/retinoic acid orphan receptor-γt (RORγt) axis.
MAIN METHODS: 100 subjects, 35 with BD and 35 with SLE in addition to 30 healthy participants were included in the study. Gene expression analysis was performed and ShinyGO database was utilized for in-depth analysis and graphical visualization of the gene ontology (GO) and pathway enrichment analysis for lncRNA and the other target genes.
KEY FINDINGS: The current results demonstrate the upregulation of lncRNA MEG3 in BD but not SLE patients. Moreover, significant differences in RORγt and FOXP3 were found between BD and SLE patients. The present findings linked lncRNA MEG3 to BD activity scores as well as CRP levels. Finally, lncRNA MEG3 showed excellent diagnostic power for BD, in addition to adequate discriminative power that can be used to differentiate between BD and SLE.
SIGNIFICANCE: The current study objectively elucidated a framework for the involvement of Treg/Th17 through transcription factors RORγt and FOXP3, in addition to their links to the downstream cytokines network including TGF-ꞵ, IL-10, IL-17 and IL-23 in BD and SLE pathogenesis and activity.