MicroRNA-155-5p regulates the Th1/Th2 cytokines expression and the apoptosis of group 2 innate lymphoid cells via targeting TP53INP1 in allergic rhinitis.

• In this study, we revealed that the TP53INP1 expression was was inversely associated with miR-155-5p in ILC2s. • MiR-155-5p disrupted the Th1/Th2 cytokines expression balance and suppressed the apoptosis of ILC2s via targeting TP53INP1 in AR. • TP53INP1 might exert its anti-inflammatory roles via inhibition NF-κB signaling pathway in AR. • Taken together, these findings suggested that miR-155-5p aggravated the inflammatory response of AR dominated by ILC2s via targeting TP53INP1, which may aid in the development of novel therapeutic agents for AR. As a key component of innate immunity, group 2 innate lymphoid cells (ILC2s) play a key role in Allergic rhinitis (AR). We previously demonstrated that both miR-155-5p and ILC2s are overexpressed in the nasal mucosa of AR patients, but the underlying mechanism remains unclear. At present study, we revealed that miR-155-5p was highly expressed in ILC2s of AR patients. Moreover, miR-155-5p promoted the secretion of Th2 cytokines of ILC2s, while inhibited the secretion of Th1 cytokines and the apoptosis of ILC2s. Meanwhile, the TP53INP1 expression was poorly expressed in ILC2s of AR patients. A dual luciferase reporter assay demonstrated that TP53INP1 was a direct target of miR-155-5p, and its expression was inversely associated with miR-155-5p in ILC2s. Furthermore, TP53INP1 inhibited the secretion of Th2 cytokines of ILC2s, while promoted the secretion of Th1 cytokines and the apoptosis of ILC2s. Notably, rescue experiments demonstrated that overexpression of TP53INP1 could partially reverse the effect of miR-155-5p on ILC2s. Taken together, these findings suggested that miR-155-5p aggravated the inflammatory response of AR dominated by ILC2s via targeting TP53INP1, which may aid in the development of novel therapeutic agents for AR. [ABSTRACT FROM AUTHOR]