IFN-beta and IFN-lambda1 Induce Kinetically Distinct Patterns of Transcription Factor Interferon Stimulated Genes in Respiratory Epithelial Cells

2015 ◽  
Vol 135 (2) ◽  
pp. AB110
Author(s):  
Lynnsey A. Renn ◽  
Terence C. Theisen ◽  
Hilary Novatt ◽  
Ronald L. Rabin
Keyword(s):  
Transcription Factor ◽  
Epithelial Cells ◽  
Respiratory Epithelial Cells ◽  
Interferon Stimulated Genes ◽  
Respiratory Epithelial

scholarly journals High dose IFN-β activates GAF to enhance expression of ISGF3 target genes in epithelial cells

2020 ◽  
Author(s):  
Kensei Kishimoto ◽  
Catera Wilder ◽  
Justin Buchanan ◽  
Minh Nguyen ◽  
Chidera Okeke ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Epithelial Cells ◽  
Target Genes ◽  
High Dose ◽  
Sequence Motifs ◽  
Respiratory Epithelial Cells ◽  
Host Immune Responses ◽  
Interferon Stimulated Genes ◽  
Respiratory Epithelial

AbstractInterferon β (IFN-β) signaling activates the transcription factor complex ISGF3 to induce gene expression programs critical for antiviral defense and host immune responses. It has also been observed that IFN-β activates a second transcription factor, γ-activated factor (GAF), but the significance of this coordinated activation is unclear. We report that in respiratory epithelial cells high doses of IFN-β indeed activate both ISGF3 and GAF, which bind to distinct genomic locations defined by their respective DNA sequence motifs. In contrast, low doses of IFN-β preferentially activate ISGF3 but not GAF. Surprisingly, in epithelial cells GAF binding does not induce nearby gene expression even when strongly bound to the promoter. Yet expression of interferon stimulated genes is enhanced when GAF and ISGF3 are both active compared to ISGF3 alone. Our data suggest that GAF enhances ISGF3 target gene expression by co-localizing with ISGF3 at some promoters and facilitating chromosome looping between distal enhancers and other promoters. We propose that GAF may function as a dose-sensitive amplifier of ISG expression to enhance antiviral immunity and establish pro-inflammatory states in respiratory epithelial cells.One sentence summaryGAF is transcriptionally inactive in epithelial cells but enhances expression of ISGF3 target genes, thus functioning as a dose-sensitive amplifier of the IFN-β response.

scholarly journals Innate antiviral cytokine response to swine influenza virus by swine respiratory epithelial cells

2021 ◽  
Author(s):  
Abhijeet Bakre ◽  
Les Jones ◽  
Jackelyn Murray ◽  
Z. Beau Reneer ◽  
Victoria Meliopoulos ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Epithelial Cells ◽  
Swine Influenza Virus ◽  
Swine Influenza ◽  
Cytokine Response ◽  
Cell Type ◽  
Respiratory Epithelial Cells ◽  
Interferon Stimulated Genes ◽  
Virus Reassortment ◽  
Respiratory Epithelial

Swine influenza virus (SIV) can cause respiratory illness in swine. Swine contribute to influenza virus reassortment as avian, human, and/or SIV viruses can infect swine, reassort, and new viruses can emerge. Thus, it is important to determine the host antiviral responses that affect SIV replication. In this study, we examined the innate antiviral cytokine response to SIV by swine respiratory epithelial cells focusing on the expression of interferon (IFN) and interferon-stimulated genes (ISGs). Both primary and transformed swine nasal and tracheal respiratory epithelial cells were examined following infection with field isolates. The results show IFN and ISG expression is maximal at 12-hour post-infection (hpi) and is cell-type and virus genotype-dependent. Importance Swine are considered intermediate hosts that have facilitated influenza virus reassortment events that have given rise pandemics or genetically related viruses have become established in swine. In this study, we examine the innate antiviral response to swine influenza virus in primary and immortalized swine nasal and tracheal epithelial cells, and show virus strain and host cell-type dependent differential expression of key interferons and interferon-stimulated genes.

scholarly journals Deletion of Forkhead Box M1 Transcription Factor from Respiratory Epithelial Cells Inhibits Pulmonary Tumorigenesis

PLoS ONE ◽  
2009 ◽  
Vol 4 (8) ◽  
pp. e6609 ◽  
Author(s):  
I-Ching Wang ◽  
Lucille Meliton ◽  
Xiaomeng Ren ◽  
Yufang Zhang ◽  
David Balli ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Epithelial Cells ◽  
Respiratory Epithelial Cells ◽  
Forkhead Box ◽  
Forkhead Box M1 ◽  
Respiratory Epithelial
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