**2.3 Other ILC2s**

According to Zhang, T2-type asthmatics showed lower airway epithelial miR-206 than normal subjects, including higher levels in type 2 hyper asthmatics than in type 2 hypo asthmatics. As a result, an animal model is built to suggest that higher miR-206 in type 2 hyper asthma can reduce CD39, an ATP degrading ectonucleotidase and a target of miR-206, whose accumulation exacerbates asthma [60]. Many cells can secrete EVs extracted from the supernatant of human mast cells (MC). Their miRNA profiling shows that miR103a-3p is markedly up-regulated and enhances IL-5 production by ILC2s after coculture with human ILC2s [61] through methylation of GATA3 arginine residues. While ICAM-1 appears to be essential for ILC2 development and function, it has been found in AR patients and animal models that overexpression of miR-150-5p can decrease ICAM-1 expression, whereas a decrease in ICAM-1 can led to a downregulation of GATA3 levels, which can, in turn, inhibit the function of ILC2s from alleviating allergic symptoms [62]. The results of an *in vivo* study in a mouse model of AR showed that miR-375 enhanced the function of ILC2s by regulating TSLP [63], providing a potential therapeutic target for AR. The miR-17 ∼ 92 gene cluster Th2 secretes related cytokines, of which miR-19a takes a significant role. By constructing a mouse model of asthma, miR-19a promoted the activation and proliferation of ILC2s, thereby increasing the secretion of IL-13 and IL-5 [51]. Roberts' study showed a biased development of ILC2s progenitors in the bone marrow of mir142−/− mice compared to wild-type mice, with a dysregulated proliferative effect of ILC2s [64]. These findings indicate that miR-142 maintains the homeostasis of ILC2s in tissues, similar to miR-155 and miR-19. With the increasing prominence of ILC2s in allergic diseases as a top research priority related to the pathogenesis of asthma to date, it is believed that further studies will undoubtedly identify additional relationships between miRNAs and ILC2s.
