ena-STUDY-HZI - HELMHOLTZ CENTRE FOR INFECTION RESEARCH, BRAUNSCHWEIG, GERMANY-21-04-2015-15:08:00:230-559
Transcriptome analysis reveals a classical interferon signature induced by IFN?4 in human primary cells.
The IFNL4 gene is negatively associated with spontaneous and treatment-induced clearance of hepatitis C virus infection. The activity of IFN?4 plays an important causal role in the pathogenesis, but the molecular details are not fully understood. One possible reason for the detrimental effect of IFN?4 could be a tissue specific regulation of an unknown subset of genes. To address both tissue- and subtype subtype-specificity in the interferon response, we treated primary human hepatocytes and airway epithelial cells with IFNa, IFN?3 or IFN?4 and assessed interferon mediated gene regulation using transcriptome sequencing. Our data show a surprisingly similar response to all three subtypes of interferon. We also addressed the tissue tissue-specificity of the response, and identified a subset of tissue tissue-specific genes. However, the interferon response is robust in both tissues with the majority of the identified genes being regulated in hepatocytes as well as airway epithelial cells. Thus we provide an in-depth analysis of the liver interferon response seen over an array of interferon subtypes and compare it to the response in the lung epithelia.
The IFNL4 gene is negatively associated with spontaneous and treatment-induced clearance of hepatitis C virus infection. The activity of IFN?4 plays an important causal role in the pathogenesis, but the molecular details are not fully understood. One possible reason for the detrimental effect of IFN?4 could be a tissue specific regulation of an unknown subset of genes. To address both tissue- and subtype subtype-specificity in the interferon response, we treated primary human hepatocytes and airway epithelial cells with IFNa, IFN?3 or IFN?4 and assessed interferon mediated gene regulation using transcriptome sequencing. Our data show a surprisingly similar response to all three subtypes of interferon. We also addressed the tissue tissue-specificity of the response, and identified a subset of tissue tissue-specific genes. However, the interferon response is robust in both tissues with the majority of the identified genes being regulated in hepatocytes as well as airway epithelial cells. Thus we provide an in-depth analysis of the liver interferon response seen over an array of interferon subtypes and compare it to the response in the lung epithelia.