Document Detail


p53 serves as a host antiviral factor that enhances innate and adaptive immune responses to influenza A virus.
MedLine Citation:
PMID:  22105999     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Several direct target genes of the p53 tumor suppressor have been identified within pathways involved in viral sensing, cytokine production, and inflammation, suggesting a potential role of p53 in antiviral immunity. The increasing need to identify immune factors to devise host-targeted therapies against pandemic influenza A virus (IAV) led us to investigate the role of endogenous wild-type p53 on the immune response to IAV. We observed that the absence of p53 resulted in delayed cytokine and antiviral gene responses in lung and bone marrow, decreased dendritic cell activation, and reduced IAV-specific CD8(+) T cell immunity. Consequently, p53(-/-) mice showed a more severe IAV-induced disease compared with their wild-type counterparts. These findings establish that p53 influences the antiviral response to IAV, affecting both innate and adaptive immunity. Thus, in addition to its established functions as a tumor suppressor gene, p53 serves as an IAV host antiviral factor that might be modulated to improve anti-IAV therapy and vaccines.
Authors:
César Muñoz-Fontela; Michael Pazos; Igotz Delgado; William Murk; Sathish Kumar Mungamuri; Sam W Lee; Adolfo García-Sastre; Thomas M Moran; Stuart A Aaronson
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-11-21
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  187     ISSN:  1550-6606     ISO Abbreviation:  J. Immunol.     Publication Date:  2011 Dec 
Date Detail:
Created Date:  2011-12-14     Completed Date:  2012-02-07     Revised Date:  2012-02-08    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  6428-36     Citation Subset:  AIM; IM    
Affiliation:
Department of Oncological Sciences, Mount Sinai School of Medicine, New York, NY 10029, USA.
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MeSH Terms
Descriptor/Qualifier:
Adaptive Immunity* / genetics
Animals
CD8-Positive T-Lymphocytes / immunology,  metabolism,  pathology
Dendritic Cells / immunology,  metabolism,  pathology
Gene Expression Regulation, Viral / immunology*
Immunity, Innate* / genetics
Influenza A Virus, H1N1 Subtype / immunology*
Influenza A Virus, H3N2 Subtype / immunology*
Male
Mice
Mice, 129 Strain
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Knockout
Mice, Transgenic
Orthomyxoviridae Infections / immunology*,  metabolism,  pathology
Pneumonia, Viral / immunology,  metabolism,  pathology
Tumor Suppressor Protein p53 / deficiency,  genetics,  physiology*
Viral Regulatory and Accessory Proteins / deficiency,  genetics,  physiology*
Grant Support
ID/Acronym/Agency:
HHS266200700010C//PHS HHS; P01 CA80058-11/CA/NCI NIH HHS; R01 AI046954/AI/NIAID NIH HHS; R01 AI41111/AI/NIAID NIH HHS; U01 AI070469/AI/NIAID NIH HHS; U01 AI082970/AI/NIAID NIH HHS; U19 AI083025/AI/NIAID NIH HHS; U54 AI057158/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/Tumor Suppressor Protein p53; 0/Viral Regulatory and Accessory Proteins

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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