LncRNA PELATON regulates Th2 cell differentiation by miR-10b-5p/GATA3 axis in allergic rhinitis.

Background: Long non-coding RNAs (lncRNAs) have been increasingly recognized as critical regulators in the pathogenesis of immunoinflammatory diseases. Nevertheless, their mechanistic contributions to Th2-driven allergic rhinitis (AR) remain unclear. This study investigated the immunomodulatory function of lncRNA PELATON in AR pathogenesis by exploring its regulatory effects on Th2 cell differentiation. Methods: A total of 32 participants were enrolled, comprising 16 patients diagnosed with AR and 16 control subjects. The allergy levels of the participants were assessed using the skin prick test (SPT), and the levels of PELATON expression in PBMCs were detected by qPCR. Spearman's correlation analysis was used to calculate the correlation between the 2 variables. Changes in GATA3, IL-4, IL-5, and IL-13 expression were examined, as well as changes in Th2 cell differentiation resulting from the overexpression of PELATON and miR-10b-5p. Modulation of miR-10b-5p and GATA3 expression by PELATON was studied via transcriptome sequencing, dual-luciferase reporter assays, and in vitro experiments. Results: LncRNA PELATON expression was elevated in patients with AR and showed a significant correlation with allergy levels. PELATON was enriched in CD4+T cells. Overexpression of PELATON in PBMCs led to an increase in the proportion of Th2 cells and the levels of GATA3, IL-4, IL-5, and IL-13 expression, while the overexpression of miR-10b-5p reduced the expression levels of GATA3, IL-4, IL-5, and IL-13. PELATON bound directly to miR-10b-5p and inhibited the negative regulatory effect of miR-10b-5p on GATA3, thereby forming a ceRNA network that promoted Th2 cell differentiation. Conclusion: LncRNA PELATON competitively binds to miR-10b-5p and promotes GATA3 expression, resulting in Th2 cell differentiation and activation in AR. Formation of the lncRNA PELATON/miR-10b-5p/GATA3 ceRNA network is a regulatory mechanism that offers new possibilities for finding therapeutic targets for AR.