[Retracted] Noncoding RNAs and Virus and Treatment in Allergic Rhinitis

Table 2

Summary of regulation and function with lncRNA in allergic rhinitis.

lncRNA	Expression	Targets	Effectors	Function
Linc00632	Down-regulated	MiR-498	IL-13 and gm-csf	Linc00632 inhibited IL-13-induced GM-CSF, eotaxin, and MUAC5AC production in IL-13-treated NECs by targeting miR-498 [44].
SNHG16	Up-regulated	miR-106-5p	Leukemia inhibitory factor (LIF) and JAK1/STAT3	SNHG16 up-regulates LIF expression by binding with miR-106b-5p, thus promoting the activity of the JAK1/STAT3 pathway and promoting cell apoptosis, inflammation, and development of AR [45].
GAS5	Up-regulated	miR-140 and niR-21	IFN-γ and IL-2	GAS5 down-regulates the expression of target proteins, including miR-140 and miR-21, accelerates the imbalance of Th1/Th2, and promotes the inflammatory response of AR patients [46].
MIAT	Up-regulated	miR-10b-5p	Th17, IL4, IL6, and IL17	MIAT can promote allergic inflammation and symptoms by activating the th17/IL4/IL6 immune response via target-inhibited miR-10b-5p in AR patients [47].
NEAT1	Up-regulated	miR-511	NR4A2 and IL13	NEAT1 induced inflammatory cytokine production and apoptosis contributing to the pathogenesis of AR via the miR-511/NR4A2 axis [48].