Resistance to viral infection of super p53 mice

Muñoz‐Fontela, César; García, María Ángel; Garcı́a-Cao, Isabel; Collado, Manuel; Arroyo, Javier; Esteban, Mariano; Serrano, Manuel; Rivas, Carmen

doi:10.1038/sj.onc.1208477

Cited by 69 publications

(63 citation statements)

References 28 publications

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“…1A), we could not rule out the possibility that p53 affects the steady-state level of other TLRs and the induction of cytokines other than IL-8, especially in light of studies proving that p53 is necessary in mounting a response against a variety of viruses, some of which may not be recognized by TLR3 (25,30). Interestingly, our preliminary investigations showed that the mRNA expression of TLR7 and TLR8 was downregulated in HCT116 p53…”

Section: Discussionmentioning

confidence: 99%

“…p53 has been implicated in the innate response to pathogens (30,31), and while TLRs are well known for mediating the recognition and response to microbial products, the relationship between p53 and TLRs is largely unexplored. To assess the involvement of p53 in TLRs' response to PAMPs, we stimulated HCT116 p53 ϩ/ϩ and p53 Ϫ/Ϫ cells with various TLR ligands, such as PGN, poly(I-C), LPS, B-DNA, and R848, and we assayed the promoter activity of IL-8, a general downstream cytokine of TLRs, in cells treated with these TLR ligands.…”

Section: Resultsmentioning

confidence: 99%

“…Several studies have highlighted the role of the transcription factor p53 in antiviral responses (7,25,30); however, the molecular mechanism remains to be clarified. Because the initiation of antiviral response is mediated, in part, by TLRs, which are important receptors that recognize microbial pathogens, we focused on the expression of TLRs and their possible regulation by p53.…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

p53 Regulates Toll-Like Receptor 3 Expression and Function in Human Epithelial Cell Lines

Taura

Eguma

Suico

et al. 2008

Molecular and Cellular Biology

113

117

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Section: Discussionmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

p53 Regulates Toll-Like Receptor 3 Expression and Function in Human Epithelial Cell Lines

Taura

Eguma

Suico

et al. 2008

Molecular and Cellular Biology

113

117

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“…TP53 gene plays a key role in the protection of host cells against viral infection and antiviral immune response (27). Polymorphisms of TP53 have been implicated in the development of a series of malignancies associated with viral infection (28)(29)(30), thyroid cancer (31), and some autoimmune diseases (32,33).…”

Section: Discussionmentioning

confidence: 99%

Herpesvirus type 7 infection may play an important role in individuals with a genetic profile of susceptibility to Graves' disease

Leite

Bufalo²,

Santos³

et al. 2010

European Journal of Endocrinology

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Objective: An inherited profile of genes related to the response to aggressive environmental factors such as viruses and chemicals may be related to an increased susceptibility to Graves' disease (GD). Design and methods: This prospective case-control study was designed to examine the relationship between human herpesviruses (HHV) infection, determined by circulating DNA; tumour protein p53 (TP53) apoptotic ability; and detoxification system genes, and GD. We studied 280 confirmed GD patients paired to 284 controls with respect to environmental exposure. Exclusion criteria included medications that could interfere with thyroid function evaluation and a recent history of viral and bacterial infections. Results: A stepwise regression analysis adjusted for age, gender, and ethnicity established the inheritance of glutathione S-transferase pi 1 (GSTP1) (odds ratio (OR)Z3.423; 95% confidence interval (CI)Z2.120-5.527; P!0.001) and cytochrome P450, family 1, subfamily A, polypeptide 1 (CYP1A1) variants (ORZ1.649; 95% CIZ1.012-2.686; PZ0.0445) as significant risk factors for the disease. HHV-7 infection was much more common in GD patients (64.64%) than in controls (38.73%; c 2 , P!0.0001), and it increased the risk for GD more than three times (ORZ3.133; 95% CIZ1.959-5.011; P!0.0001). The inheritance of less efficient Pro/Pro TP53 gene variants significantly increased the risk of GD development (ORZ5.196;; P!0.0001) and also favored HHV-7 infection (ORZ2.835; 95% CIZ1.100-7.310; PZ0.0275). In addition, 72TP53 variants augmented the risk of GD relapse (ORZ1.860; 95% CIZ1.015-3.410; PZ0.0446). Conclusions: We suggest that an inherited genetic profile involving TP53 may favor HHV-7 infection and maintenance, which, in turn, may initiate and perpetuate GD autoimmune process.

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“…87 The number of identified cellular functions that p53 regulates has greatly increased over the past few years, and there is now a vast array of evidence that shows that p53 can be induced by viral infection 88 to limit pathogen spread by inducing apoptosis. 89,90 Furthermore, p53 not only acts as an intrinsic barrier against tumorigenesis or pathogenic spread but can also lead to increased cellular immunogenicity. For example, p53 reactivation in a hepatocellular carcinoma can promote tumor regression mediated by innate immunity.…”

Section: Senescencementioning

confidence: 99%

Molecular mechanisms of natural killer cell activation in response to cellular stress

2013

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Protection against cellular stress from various sources, such as nutritional, physical, pathogenic, or oncogenic, results in the induction of both intrinsic and extrinsic cellular protection mechanisms that collectively limit the damage these insults inflict on the host. The major extrinsic protection mechanism against cellular stress is the immune system. Indeed, it has been well described that cells that are stressed due to association with viral infection or early malignant transformation can be directly sensed by the immune system, particularly natural killer (NK) cells. Although the ability of NK cells to directly recognize and respond to stressed cells is well appreciated, the mechanisms and the breadth of cell-intrinsic responses that are intimately linked with their activation are only beginning to be uncovered. This review will provide a brief introduction to NK cells and the relevant receptors and ligands involved in direct responses to cellular stress. This will be followed by an in-depth discussion surrounding the various intrinsic responses to stress that can naturally engage NK cells, and how therapeutic agents may induce specific activation of NK cells and other innate immune cells by activating cellular responses to stress.

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Resistance to viral infection of super p53 mice

Cited by 69 publications

References 28 publications

p53 Regulates Toll-Like Receptor 3 Expression and Function in Human Epithelial Cell Lines

p53 Regulates Toll-Like Receptor 3 Expression and Function in Human Epithelial Cell Lines

Herpesvirus type 7 infection may play an important role in individuals with a genetic profile of susceptibility to Graves' disease

Molecular mechanisms of natural killer cell activation in response to cellular stress

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