Journal
JOURNAL OF IMMUNOLOGY
Volume 187, Issue 12, Pages 6428-6436Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1101459
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Funding
- National Institutes of Health [P01 CA80058-11, R01 AI046954, U01 AI070469, U19 AI083025, U54 AI057158, U01 AI082970, R01 AI41111]
- Center for Research on Influenza Pathogenesis, a National Institute of Allergy and Infectious Diseases-supported center [HHS266200700010C]
- Basque government
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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 wildtype 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. The Journal of Immunology, 2011, 187: 6428-6436.
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