Epigenetic silencing of IRF1 dysregulates type III interferon responses to respiratory virus infection in epithelial to mesenchymal transition

• Published in: Nature microbiology Vol. 2; no. 8; p. 17086
• Main Authors: Yang, Jun, Tian, Bing, Sun, Hong, Garofalo, Roberto P., Brasier, Allan R.
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 05.06.2017; Nature Publishing Group
• Subjects: 14; 14/63; 38; 38/77; 42; 42/41; 631/250/262; 631/326/596/2555; 631/326/596/2557; 64; 64/60; 692/420/254; Allergic diseases; Antiviral Agents - metabolism; Cells, Cultured; Chronic infection; Epigenesis, Genetic; Epigenetics; Epithelial Cells - physiology; Epithelial Cells - virology; Epithelial-Mesenchymal Transition; Fibrosis; Gene Silencing; Homeobox; Host-Pathogen Interactions; Humans; Immune Evasion; Infectious Diseases; Interferon; Interferon regulatory factor; Interferon regulatory factor 1; Interferon regulatory factor 3; Interferon Regulatory Factor-1 - biosynthesis; Interferons - metabolism; Life Sciences; Medical Microbiology; Mesenchyme; Microbiology; Mucosa; Parasitology; Polycomb group proteins; Respiratory syncytial virus; Respiratory Syncytial Viruses - physiology; Respiratory tract diseases; Rhinovirus; Transforming growth factor-b; Virology; Zinc Finger E-box-Binding Homeobox 1 - metabolism; Zinc finger proteins

Chronic oxidative injury produced by airway disease triggers a transforming growth factor-β (TGF-β)-mediated epigenetic reprogramming known as the epithelial–mesenchymal transition (EMT). We observe that EMT silences protective mucosal interferon (IFN)-I and III production associated with enhanced r...