LncRNA JPX contributes to Treg/Th17 imbalance in allergic rhinitis via targeting the miR-378g/CCL5 axis

• Published in: Immunopharmacology and immunotoxicology Vol. 44; no. 4; pp. 519 - 524
• Main Authors: Chen, Ziqi, Ke, Xia, Wang, Xiaoqiang, Kang, Houyong, Hong, Suling
• Format: Journal Article
• Language: English
• Published: Taylor & Francis 04.07.2022
• Subjects: Allergic rhinitis; CCL5; lncRNA JPX; miR-378g; Treg/Th17
• ISSN: 0892-3973; 1532-2513; 1532-2513
• DOI: 10.1080/08923973.2022.2055566

Aim: T-regulatory (Treg)/T-helper (Th) 17 imbalance contributes to the pathogenesis of allergic rhinitis (AR). Long non-coding RNAs (lncRNAs) participate in the progression of AR. Herein, the effect of lncRNA JP X on Treg/Th17 balance in AR was explored. Methods: CD4+ T cells were isolated from patients with AR and healthy control. The percentage of Treg and Th17 cells were examined by flow cytometry. The levels of JP X, miR-378g, CCL5, T GF-β, and IL-17A were tested using qRT-P CR. The protein expression of Foxp3 and RORγt was measured by western blot. Results: The data showed that an imbalance of Treg/Th17 was associated with AR. Upregulation of JP X was found in AR, and knockdown of which improved the imbalance of Treg/Th17. Furthermore, JP X functioned as a sponge of miR-378g to upregulate CCL5. Inhibition of miR-378g reversed the effects on Treg/Th17 induced by silencing of JP X. Moreover, overexpression of CCL5 reversed miR-378g-induced effects. Conclusion: In conclusion, depletion of JP X promoted Treg/Th17 balance in AR via regulating the miR-378g/CCL5 axis. The findings provided a novel therapeutic insight for AR.