miR103a-3p in extracellular vesicles from FcεRI-aggregated human mast cells enhances IL-5 production by group 2 innate lymphoid cells

BackgroundMast cells (MCs) are key regulators of IgE-mediated allergic inflammation. Cell-derived extracellular vesicles (EVs) contain bioactive compounds such as microRNAs. EVs can transfer signals to recipient cells, thus using a novel mechanism cell-to-cell communication. However, whether MC-derived involved in FcεRI-mediated inflammation is unclear.ObjectiveWe sought investigate the effect derived from FcεRI-aggregated human MCs on function group 2 innate lymphoid (ILC2s).MethodsHuman cultured were sensitized with and without IgE for 1 hour then incubated anti-IgE antibody, IL-33, or medium alone 24 hours. MC supernatant isolated by ExoQuick-TC.ResultsCoculture ILC2s significantly enhanced IL-5 production sustained upregulation mRNA expression IL-33–stimulated ILC2s, but IL-13 unchanged. miR103a-3p was upregulated that had been cocultured antibody–stimulated MCs. Transduction an mimic ILC2s. promoted demethylation arginine residue GATA3 downregulating protein methyltransferase 5 (PRMT5) mRNA. Reduction small interfering RNA technique resulted Furthermore, level higher sera patients atopic dermatitis than nonatopic healthy control subjects.ConclusionEosinophilic may be exacerbated owing ILC2 activation miR103a-3p. Mast unclear. We (ILC2s). Human ExoQuick-TC. Coculture subjects. Eosinophilic