MicroRNA-21–Eosinophil Cationic Protein–Interleukin-4 signaling network (miR-21–ECP–IL-4) (miR-21–ECP–IL-4)

The MicroRNA-21–Eosinophil Cationic Protein–Interleukin-4 (miR-21–ECP–IL-4) signaling network is a regulatory axis central to the pathophysiology of Type 2 (Th2)-high inflammatory conditions, most notably eosinophilic asthma. MicroRNA-21 (miR-21) functions as a key epigenetic modulator that promotes Th2 cell polarization and the subsequent secretion of Interleukin-4 (IL-4), a cytokine essential for B-cell IgE switching and eosinophil recruitment (Elbehidy et al., 2016). Activated eosinophils release Eosinophil Cationic Protein (ECP), a cytotoxic ribonuclease that mediates airway epithelial damage and contributes to bronchial hyperreactivity (NIH/PubMed). Research indicates that miR-21 levels are significantly elevated in the serum and sputum of asthmatic patients, where they positively correlate with IL-4 and ECP concentrations, especially in cases of steroid-resistant asthma (Lu et al., 2009). Therapeutic intervention targeting this network includes the use of IL-4 receptor antagonists like dupilumab and experimental anti-miR-21 oligonucleotides, which aim to resolve chronic airway inflammation and prevent tissue remodeling.

Other names

miR-21/ECP/IL-4 axisMicroRNA-21/Eosinophil Cationic Protein/Interleukin-4 pathwaymiR-21-mediated Th2 signaling network

MicroRNA-21 (miR-21) promotes the polarization of naive T cells into Th2 cells and enhances the production of Interleukin-4 (IL-4). IL-4 subsequently drives the recruitment and activation of eosinophils, which release Eosinophil Cationic Protein (ECP), leading to tissue damage and airway hyperresponsiveness.