**1.6 Other related miRNAs**

Analysis of clinical data identified that children with asthma presented with reduced levels of miR-34a, miR-92b, and miR-210 secretion from airway epithelial extracellular vesicle (EV), while the decline may enable DCs to polarize Th2 cells, giving rise to the asthma phenotype [46]. The extraction of lymphocytes from asthmatic children yielded significantly lower levels of miR-451a than baseline, miRNA-451a with an FC of 4.6 and a p-value of 0.008 (asthma vs. control), and down-regulation of miR-451a was observed when CD4+ T cells were placed in Th2 differentiation medium and ETS1 upregulation, leading to the evidence that miRNA-451 inhibits Th2 differentiation by downregulating EST1 [47]. Furthermore, a significant reduction in type 2 allergic lung inflammation was observed in asthma model mice with upregulation of miR-1165-3p in mouse lung tissue, suggesting that miR-1165-3p could inhibit Th2 differentiation, which was achieved by directly targeting IL-13 and PPM1A [48]. In addition, miR-29b upregulation in an asthma model can modify the Th1/Th2 balance by inhibiting ICOS expression, thereby attenuating eosinophil recruitment

in airway epithelial cells [49]. MiRNAs have a profound impact on the regulation of allergic inflammation and are expected to become biomarkers for allergic diseases, such as asthma, as well as important therapeutic targets in the future. MiRNAs with a profound impact on the regulation of allergic inflammation are expected to be biomarkers for allergic diseases, such as asthma, and may likewise be a valuable therapeutic target in the future.
