Dual Role of p53 in Innate Antiviral Immunity

Viruses

Carmen Rivas¹  Stuart A. Aaronson² 

[1] Centro Nacional de Biotecnologia, CSIC, Darwin 3, Campus Universidad Autónoma, Madrid 28049, Spain; E-Mail: [e-mail] (C.R.);Department of Oncological Sciences, Mount Sinai School of Medicine, One Gustave L. Levy Place Box 1130, New York, NY 10029, USA; E-Mail: [e-mail] (S.A.A.)

关键词: p53;    interferon;    immunity;    apoptosis;   

DOI  :  10.3390/v2010298

来源: mdpi

【 摘 要 】

Tumor suppressor p53 is widely known as ‘the guardian of the genome’ due to its ability to prevent the emergence of transformed cells by the induction of cell cycle arrest and apoptosis. However, recent studies indicate that p53 is also a direct transcriptional target of type I interferons (IFNs) and thus, it is activated by these cytokines upon viral infection. p53 has been shown to contribute to virus-induced apoptosis, therefore dampening the ability of a wide range of viruses to replicate and spread. Interestingly, recent studies also indicate that several IFN-inducible genes such as interferon regulatory factor 9 (IRF9), IRF5, IFN-stimulated gene 15 (ISG15) and toll-like receptor 3 (TLR3) are in fact, p53 direct transcriptional targets. These findings indicate that p53 may play a key role in antiviral innate immunity by both inducing apoptosis in response to viral infection, and enforcing the type I IFN response, and provide a new insight into the evolutionary reasons why many viruses encode p53 antagonistic proteins.

【 授权许可】

CC BY   
© 2010 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland