Interferon‐γ stimulates p11‐dependent surface expression of annexin A2 in lung epithelial cells to enhance phagocytosis

摘要: Annexin A2 (p36) is usually present together with its natural ligand p11 as a heterotetramer complex, which has multiple biological functions depending on cellular localization. However, the detailed mechanism of annexin translocation and physiological role in inflammation remain unclear. Here, we show that IFN-γ stimulation enhances surface lung epithelial cells. While total protein remains unchanged, expression upregulated via IFN-γ-activated JAK2/STAT1 signal pathway. Notably, IFN-γ-induced required for to cell surface. Since lacks peptide by classical endoplasmic reticulum-Golgi route, mode trafficking We observed p11-dependent associated exosomal secretion The increase exosomes blocked p11-silenced Furthermore, mediates phagocytosis apoptotic cells These findings provide insights into illustrate pivotal function phagocytic response IFN-γ.