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Development and Validation of an Ultrasensitive Single Molecule Array Digital Enzyme-linked Immunosorbent Assay for Human Interferon-α
Published on: June 14, 2018
Transcriptome analysis reveals a classical interferon signature induced by IFNλ4 in human primary cells
C Lauber1, G Vieyres2, E Terczyńska-Dyla3
1Institute for Medical Informatics and Biometry, Technische Universität Dresden, Dresden, Germany.
Abstract:
The IFNL4 gene is negatively associated with spontaneous and treatment-induced clearance of hepatitis C virus infection. The activity of IFNλ4 has an important causal role in the pathogenesis, but the molecular details are not fully understood. One possible reason for the detrimental effect of IFNλ4 could be a tissue-specific regulation of an unknown subset of genes. To address both tissue and subtype specificity in the interferon response, we treated primary human hepatocytes and airway epithelial cells with IFNα, IFNλ3 or IFNλ4 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 specificity of the response, and identified a subset of 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 epithelium.
Insights
Interferon lambda 4 (IFNλ4) may worsen hepatitis C, but this study found IFNλ4, IFNλ3, and IFNα trigger similar gene responses in liver and lung cells, challenging prior assumptions.
Area of Science:
- Immunology
- Hepatology
- Molecular Biology
Background:
- The IFNL4 gene is linked to poorer outcomes in Hepatitis C Virus (HCV) infection, suggesting a role in pathogenesis.
- The precise molecular mechanisms behind IFNλ4's detrimental effects, potentially involving tissue-specific gene regulation, remain unclear.
Purpose of the Study:
- To investigate the tissue and subtype specificity of interferon responses.
- To compare the gene regulation patterns induced by IFNα, IFNλ3, and IFNλ4 in primary human hepatocytes and airway epithelial cells.
Main Methods:
- Primary human hepatocytes and airway epithelial cells were treated with IFNα, IFNλ3, or IFNλ4.
- Transcriptome sequencing was employed to analyze interferon-mediated gene regulation.
Main Results:
- All three interferon subtypes (IFNα, IFNλ3, IFNλ4) induced largely similar gene expression patterns.
- A subset of tissue-specific genes was identified, but the interferon response was robust in both hepatocytes and airway epithelial cells.
- The majority of regulated genes showed similar responses in both liver and lung cells.
Conclusions:
- The interferon response to IFNα, IFNλ3, and IFNλ4 is broadly conserved across liver and lung epithelial cells.
- IFNλ4's detrimental role in HCV pathogenesis may not stem from unique tissue-specific gene regulation compared to other interferon subtypes.
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