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High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes
Published on: March 24, 2015
Integrin alpha 11 is a novel type I interferon stimulated gene
Luiz Felipe Leomil Coelho1, Bruno Eduardo Fernandes Mota, Paula Cristiane Motta Sales
1Laboratório de Vírus, Departamento de Microbiologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Cytokine
|May 16, 2006
Summary
Interferons (IFNs) induce integrin alpha 11 (ITGA-11) expression in cells and mice. This study reveals ITGA-11 as a novel interferon stimulated gene, regulated by protein kinase R (PKR).
Area of Science:
- Immunology
- Molecular Biology
- Cell Biology
Background:
- Interferons (IFNs) are crucial cytokines regulating cellular functions and immunity.
- Type I IFNs (IFN-alpha, IFN-beta) and Type II IFNs (IFN-gamma) mediate distinct biological activities.
- Interferon stimulated genes (ISGs) are induced by IFNs to execute their functions.
Purpose of the Study:
- To determine if integrin alpha 11 (ITGA-11), a collagen-binding integrin, is induced by Type I IFNs.
- To elucidate the role of protein kinase R (PKR) in ITGA-11 induction by IFNs.
Main Methods:
- Investigated ITGA-11 mRNA and protein levels in T98G cells and BALB/c mice following Type I IFN treatment.
- Analyzed ITGA-11 expression in T98G cells infected with Murine encephalomyocarditis virus.
- Utilized PKR-deficient mouse embryo fibroblasts (MEFs) to assess PKR's role in IFN-induced ITGA-11 expression.
Main Results:
- Type I IFNs significantly increased ITGA-11 mRNA and protein levels in T98G cells.
- In vivo studies showed ITGA-11 induction in the spleen and lungs of IFN-treated mice.
- PKR deficiency abolished IFN-induced ITGA-11 expression, indicating PKR dependence.
- ITGA-11 promoter analysis revealed potential IFN-regulated transcription factor binding sites.
Conclusions:
- Integrin alpha 11 (ITGA-11) is a novel interferon stimulated gene (ISG).
- ITGA-11 induction by Type I IFNs is dependent on the protein kinase R (PKR) pathway.
- These findings expand the understanding of IFN signaling pathways and their targets.
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