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

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.</p

Frequencies of the haplotypes formed by rs17375018, rs7517847, rs1343151 and rs11209032 SNPs in AR patients and healthy control individuals.

<p>AR, allergic rhinitis; OR, odds ratio.</p

Frequencies of alleles and genotypes of IL-23R polymorphisms in AR patients and control individuals.

<p>AR, allergic rhinitis; OR, odds ratio; SNP, single-nucleotide polymorphism.</p><p>Logistic regression analysis was used to analyze the genotype allele controlling for age, gender and occupation as the covariables.</p

The 4 SNP call rates in patients and control individuals and HWE p-values.

<p>AR, allergic rhinitis, SNP; single-nucleotide polymorphism; HWE,Hardy-Weinberg equilibrium.</p

Clinical features and demographic characteristics of the study population.

<p>AR, allergic rhinitis.</p