Fig. 6From: Interferon gamma induces inflammatory responses through the interaction of CEACAM1 and PI3K in airway epithelial cellsPotential mechanism of CEACAM1 and PI3K interactions. In the infectious environment during acute exacerbation of COPD, the increased IFN-γ up-regulated the expression of CEACAM1, especially the -S isoforms, which further promotes cellular migration, proliferation and induces the production of inflammatory factors such as IL-6 and IL-8. The -L isoforms of CEACAM1 contains two ITIMs in the cytoplasmic tail, which negatively regulates down-stream signal transduction pathways. PI3K/Akt pathway inhibitors (GDC0941, CAL101, LY294002, SHBM1009, BEZ235 and GSK69063) inhibited CAECAM1 expression, which suggested that PI3K/Akt pathway induces the up-regulation of CEACAM1 after IFN-γ stimulation. Different from other PI3K/Akt pathway inhibitors, SHBM1009 could specifically up regulate CEACAM1-L isoforms. As a positive feedback, CEACAM1 promoted the activation of PI3K/Akt pathwayBack to article page