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Functional characterization of goose IRF1 in IFN induction and anti-NDV infection
Interferon regulatory factors (IRFs) play a key role in many aspects of immune response, and IRF1, IRF3, and IRF7 are positive regulators of IFN induction in mammals. However, IRF3, as the most critical regulatory factor in mammals, is naturally absent in birds, which attracts us to study the functi...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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BioMed Central
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8981851/ https://www.ncbi.nlm.nih.gov/pubmed/35379320 http://dx.doi.org/10.1186/s13567-022-01046-9 |
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author | Lin, Zhenyu Wang, Jie Zhang, Nian Yi, Jianshu Wang, Zhaofei Ma, Jingjiao Wang, Hengan Yan, Yaxian Qian, Kun Sun, Jianhe Cheng, Yuqiang |
author_facet | Lin, Zhenyu Wang, Jie Zhang, Nian Yi, Jianshu Wang, Zhaofei Ma, Jingjiao Wang, Hengan Yan, Yaxian Qian, Kun Sun, Jianhe Cheng, Yuqiang |
author_sort | Lin, Zhenyu |
collection | PubMed |
description | Interferon regulatory factors (IRFs) play a key role in many aspects of immune response, and IRF1, IRF3, and IRF7 are positive regulators of IFN induction in mammals. However, IRF3, as the most critical regulatory factor in mammals, is naturally absent in birds, which attracts us to study the functions of other members of the avian IRF family. In the present study, we cloned goose IRF1 (GoIRF1) and conducted a series of bioinformatics analyses to compare the protein homology of GoIRF1 with that of IRF1 in other species. The overexpression of GoIRF1 in DF-1 cells induced the activation of IFN-β, and this activation is independent of the dosage of the transfected GoIRF1 plasmids. The overexpression of GoIRF1 in goose embryonic fibroblasts (GEFs) induced the expression of IFNs, proinflammatory cytokines, and IFN-stimulated genes (ISGs); it also inhibited the replication of green fluorescent protein (GFP)-tagged Newcastle disease virus (NDV) (NDV-GFP) and GFP-tagged vesicular stomatitis virus (VSV) (VSV-GFP). Our results suggest that GoIRF1 is an important regulator of IFNs, proinflammatory cytokines, and ISGs and plays a role in antiviral innate immunity in geese. |
format | Online Article Text |
id | pubmed-8981851 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-89818512022-04-06 Functional characterization of goose IRF1 in IFN induction and anti-NDV infection Lin, Zhenyu Wang, Jie Zhang, Nian Yi, Jianshu Wang, Zhaofei Ma, Jingjiao Wang, Hengan Yan, Yaxian Qian, Kun Sun, Jianhe Cheng, Yuqiang Vet Res Research Article Interferon regulatory factors (IRFs) play a key role in many aspects of immune response, and IRF1, IRF3, and IRF7 are positive regulators of IFN induction in mammals. However, IRF3, as the most critical regulatory factor in mammals, is naturally absent in birds, which attracts us to study the functions of other members of the avian IRF family. In the present study, we cloned goose IRF1 (GoIRF1) and conducted a series of bioinformatics analyses to compare the protein homology of GoIRF1 with that of IRF1 in other species. The overexpression of GoIRF1 in DF-1 cells induced the activation of IFN-β, and this activation is independent of the dosage of the transfected GoIRF1 plasmids. The overexpression of GoIRF1 in goose embryonic fibroblasts (GEFs) induced the expression of IFNs, proinflammatory cytokines, and IFN-stimulated genes (ISGs); it also inhibited the replication of green fluorescent protein (GFP)-tagged Newcastle disease virus (NDV) (NDV-GFP) and GFP-tagged vesicular stomatitis virus (VSV) (VSV-GFP). Our results suggest that GoIRF1 is an important regulator of IFNs, proinflammatory cytokines, and ISGs and plays a role in antiviral innate immunity in geese. BioMed Central 2022-04-04 2022 /pmc/articles/PMC8981851/ /pubmed/35379320 http://dx.doi.org/10.1186/s13567-022-01046-9 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Article Lin, Zhenyu Wang, Jie Zhang, Nian Yi, Jianshu Wang, Zhaofei Ma, Jingjiao Wang, Hengan Yan, Yaxian Qian, Kun Sun, Jianhe Cheng, Yuqiang Functional characterization of goose IRF1 in IFN induction and anti-NDV infection |
title | Functional characterization of goose IRF1 in IFN induction and anti-NDV infection |
title_full | Functional characterization of goose IRF1 in IFN induction and anti-NDV infection |
title_fullStr | Functional characterization of goose IRF1 in IFN induction and anti-NDV infection |
title_full_unstemmed | Functional characterization of goose IRF1 in IFN induction and anti-NDV infection |
title_short | Functional characterization of goose IRF1 in IFN induction and anti-NDV infection |
title_sort | functional characterization of goose irf1 in ifn induction and anti-ndv infection |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8981851/ https://www.ncbi.nlm.nih.gov/pubmed/35379320 http://dx.doi.org/10.1186/s13567-022-01046-9 |
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