Nuclear Factor κB2 p52 Protein Has a Role in Antiviral Immunity through IκB Kinase ϵ-dependent Induction of Sp1 Protein and Interleukin 15

In this study we describe a previously unreported function for NFκB2, an NFκB family transcription factor, in antiviral immunity. NFκB2 is induced in response to poly(I:C), a mimic of viral dsRNA. Poly(I:C), acting via TLR3, induces p52-dependent transactivation of a reporter gene in a manner that r...

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Published inThe Journal of biological chemistry Vol. 288; no. 35; pp. 25066 - 25075
Main Authors Doyle, Sarah L., Shirey, Kari Ann, McGettrick, Anne F., Kenny, Elaine F., Carpenter, Susan, Caffrey, Brian E., Gargan, Siobhan, Quinn, Susan R., Caamaño, Jorge H., Moynagh, Paul, Vogel, Stefanie N., O'Neill, Luke A.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 30.08.2013
American Society for Biochemistry and Molecular Biology
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Sp1
Sp1
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Abstract In this study we describe a previously unreported function for NFκB2, an NFκB family transcription factor, in antiviral immunity. NFκB2 is induced in response to poly(I:C), a mimic of viral dsRNA. Poly(I:C), acting via TLR3, induces p52-dependent transactivation of a reporter gene in a manner that requires the kinase activity of IκB kinase ϵ (IKKϵ) and the transactivating potential of RelA/p65. We identify a novel NFκB2 binding site in the promoter of the transcription factor Sp1 that is required for Sp1 gene transcription activated by poly(I:C). We show that Sp1 is required for IL-15 induction by both poly(I:C) and respiratory syncytial virus, a response that also requires NFκB2 and IKKϵ. Our study identifies NFκB2 as a target for IKKϵ in antiviral immunity and describes, for the first time, a role for NFκB2 in the regulation of gene expression in response to viral infection. Background: IKKϵ can promote the ability of p52 to transactivate gene expression in a manner requiring p65. Results: p52 is induced by TLR3 activation and regulates Sp1 transcription. Sp1 promotes the transcription of IL-15. Both events require the presence of IKKϵ and p52. Conclusion: p52 is a target for IKKϵ in antiviral immunity. Significance: This study reports a role for NFκB2 in the induction of antiviral gene expression.
AbstractList In this study we describe a previously unreported function for NFκB2, an NFκB family transcription factor, in antiviral immunity. NFκB2 is induced in response to poly(I:C), a mimic of viral dsRNA. Poly(I:C), acting via TLR3, induces p52-dependent transactivation of a reporter gene in a manner that requires the kinase activity of IκB kinase ε (IKKε) and the transactivating potential of RelA/p65. We identify a novel NFκB2 binding site in the promoter of the transcription factor Sp1 that is required for Sp1 gene transcription activated by poly(I:C). We show that Sp1 is required for IL-15 induction by both poly(I:C) and respiratory syncytial virus, a response that also requires NFκB2 and IKKε. Our study identifies NFκB2 as a target for IKKε in antiviral immunity and describes, for the first time, a role for NFκB2 in the regulation of gene expression in response to viral infection.
Background: IKKϵ can promote the ability of p52 to transactivate gene expression in a manner requiring p65. Results: p52 is induced by TLR3 activation and regulates Sp1 transcription. Sp1 promotes the transcription of IL-15. Both events require the presence of IKKϵ and p52. Conclusion: p52 is a target for IKKϵ in antiviral immunity. Significance: This study reports a role for NFκB2 in the induction of antiviral gene expression. In this study we describe a previously unreported function for NFκB2, an NFκB family transcription factor, in antiviral immunity. NFκB2 is induced in response to poly(I:C), a mimic of viral dsRNA. Poly(I:C), acting via TLR3, induces p52-dependent transactivation of a reporter gene in a manner that requires the kinase activity of IκB kinase ϵ (IKKϵ) and the transactivating potential of RelA/p65. We identify a novel NFκB2 binding site in the promoter of the transcription factor Sp1 that is required for Sp1 gene transcription activated by poly(I:C). We show that Sp1 is required for IL-15 induction by both poly(I:C) and respiratory syncytial virus, a response that also requires NFκB2 and IKKϵ. Our study identifies NFκB2 as a target for IKKϵ in antiviral immunity and describes, for the first time, a role for NFκB2 in the regulation of gene expression in response to viral infection.
In this study we describe a previously unreported function for NFκB2, an NFκB family transcription factor, in antiviral immunity. NFκB2 is induced in response to poly(I:C), a mimic of viral dsRNA. Poly(I:C), acting via TLR3, induces p52-dependent transactivation of a reporter gene in a manner that requires the kinase activity of IκB kinase ϵ (IKKϵ) and the transactivating potential of RelA/p65. We identify a novel NFκB2 binding site in the promoter of the transcription factor Sp1 that is required for Sp1 gene transcription activated by poly(I:C). We show that Sp1 is required for IL-15 induction by both poly(I:C) and respiratory syncytial virus, a response that also requires NFκB2 and IKKϵ. Our study identifies NFκB2 as a target for IKKϵ in antiviral immunity and describes, for the first time, a role for NFκB2 in the regulation of gene expression in response to viral infection. Background: IKKϵ can promote the ability of p52 to transactivate gene expression in a manner requiring p65. Results: p52 is induced by TLR3 activation and regulates Sp1 transcription. Sp1 promotes the transcription of IL-15. Both events require the presence of IKKϵ and p52. Conclusion: p52 is a target for IKKϵ in antiviral immunity. Significance: This study reports a role for NFκB2 in the induction of antiviral gene expression.
Author Moynagh, Paul
Doyle, Sarah L.
Caamaño, Jorge H.
Quinn, Susan R.
O'Neill, Luke A.
Shirey, Kari Ann
Carpenter, Susan
McGettrick, Anne F.
Caffrey, Brian E.
Gargan, Siobhan
Vogel, Stefanie N.
Kenny, Elaine F.
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Issue 35
Keywords Gene Regulation
Cytokine Induction
NF-κB
Molecular Biology
Signal Transduction
Transcription
Sp1
Innate Immunity
Viral Immunology
Toll-like Receptor (TLR)
Language English
License This is an open access article under the CC BY license.
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Notes Both authors contributed equally to this work.
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Snippet In this study we describe a previously unreported function for NFκB2, an NFκB family transcription factor, in antiviral immunity. NFκB2 is induced in response...
Background: IKKϵ can promote the ability of p52 to transactivate gene expression in a manner requiring p65. Results: p52 is induced by TLR3 activation and...
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SubjectTerms Animals
Cytokine Induction
Gene Expression Regulation - drug effects
Gene Expression Regulation - genetics
Gene Expression Regulation - immunology
Gene Regulation
HEK293 Cells
Humans
I-kappa B Kinase - genetics
I-kappa B Kinase - immunology
I-kappa B Kinase - metabolism
Innate Immunity
Interferon Inducers - pharmacology
Interleukin-15 - genetics
Interleukin-15 - metabolism
Mice
Mice, Knockout
Molecular Biology
NF-kappa B p52 Subunit - genetics
NF-kappa B p52 Subunit - immunology
NF-kappa B p52 Subunit - metabolism
NF-κB
Poly I-C - pharmacology
Respiratory Syncytial Virus Infections - genetics
Respiratory Syncytial Virus Infections - immunology
Respiratory Syncytial Virus Infections - metabolism
Respiratory Syncytial Virus Infections - pathology
Respiratory Syncytial Viruses - genetics
Respiratory Syncytial Viruses - immunology
Respiratory Syncytial Viruses - metabolism
Response Elements - genetics
Response Elements - immunology
Signal Transduction
Sp1
Sp1 Transcription Factor - biosynthesis
Sp1 Transcription Factor - genetics
Sp1 Transcription Factor - immunology
Toll-like Receptor (TLR)
Toll-Like Receptor 3 - genetics
Toll-Like Receptor 3 - immunology
Toll-Like Receptor 3 - metabolism
Transcription
Transcription Factor RelA - genetics
Transcription Factor RelA - immunology
Transcription Factor RelA - metabolism
Viral Immunology
Title Nuclear Factor κB2 p52 Protein Has a Role in Antiviral Immunity through IκB Kinase ϵ-dependent Induction of Sp1 Protein and Interleukin 15
URI https://dx.doi.org/10.1074/jbc.M113.469122
https://www.ncbi.nlm.nih.gov/pubmed/23873932
https://pubmed.ncbi.nlm.nih.gov/PMC3757171
Volume 288
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