ArticleJournal of virology2017
UV Radiation Activates Toll-Like Receptor 9 Expression in Primary Human Keratinocytes, an Event Inhibited by Human Papillomavirus 38 E6 and E7 Oncoproteins.
Article in Journal of virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- Genetic Engineering of Human Keratinocytes Using CRISPR/Cas9 Ribonucleoprotein Complexes or Modified Cas9-Encoding mRNAs.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Patterns of immune cell infiltration and oxidative stress in cervical cancer.Oncology reviews · 2025Review
- TLR9 activation in large wound induces tissue repair and hair follicle regeneration via γδT cells.Cell death & disease · 2024Article
- HPV38 impairs UV-induced transcriptional activation of the IL-18 pro-inflammatory cytokine.mSphere · 2023Article
- Review
- Synonymous nucleotide changes drive papillomavirus evolution.Tumour virus research · 2022Review
- Human Beta Papillomavirus Type 8 E1 and E2 Proteins Suppress the Activation of the RIG-I-Like Receptor MDA5.Viruses · 2022Article
- Article
- Merkel Cell Polyoma Virus and Cutaneous Human Papillomavirus Types in Skin Cancers: Optimal Detection Assays, Pathogenic Mechanisms, and Therapeutic Vaccination.Pathogens (Basel, Switzerland) · 2022Review
- Human Papillomavirus and carcinogenesis: Novel mechanisms of cell communication involving extracellular vesicles.Cytokine & growth factor reviews · 2020Review
- Photoimmunology: how ultraviolet radiation affects the immune system.Nature reviews. Immunology · 2019Review
- Significance and Role of Pattern Recognition Receptors in Malignancy.Archivum immunologiae et therapiae experimentalis · 2019Review
- Cross-talk of cutaneous beta human papillomaviruses and the immune system: determinants of disease penetrance.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019Review
- E6/E7 and E6Frontiers in immunology · 2019Article
- Long Sun-Exposures Influencing High Sub-Cutaneous Synthesis of Vitamin-D3 may be Associated with Exacerbation of Symptoms in Allergic-Asthma.The journal of aging research & clinical practice · 2018Article
- Cutaneous Papillomaviruses and Non-melanoma Skin Cancer: Causal Agents or Innocent Bystanders?Frontiers in microbiology · 2018Review
- Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Several lines of evidence indicate that cutaneous human papillomavirus (HPV) types belonging to the beta genus of the HPV phylogenetic tree synergize with UV radiation in the development of skin cancer. Accordingly, the E6 and E7 oncoproteins from some beta HPV types are able to deregulate pathways related to immune response and cellular transformation. Toll-like receptor 9 (TLR9), in addition to playing a role in innate immunity, has been shown to be involved in the cellular stress response. Using primary human keratinocytes as experimental models, we have shown that UV irradiation (and other cellular stresses) activates TLR9 expression. This event is closely linked to p53 activation. Silencing the expression of p53 or deleting its encoding gene affected the activation of TLR9 expression after UV irradiation. Using various strategies, we have also shown that the transcription factors p53 and c-Jun are recruited onto a specific region of the TLR9 promoter after UV irradiation. Importantly, the E6 and E7 oncoproteins from beta HPV38, by inducing the accumulation of the p53 antagonist ΔNp73α, prevent the UV-mediated recruitment of these transcription factors onto the TLR9 promoter, with subsequent impairment of TLR9 gene expression. This study provides new insight into the mechanism that mediates TLR9 upregulation in response to cellular stresses. In addition, we show that HPV38 E6 and E7 are able to interfere with this mechanism, providing another explanation for the possible cooperation of beta HPV types with UV radiation in skin carcinogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.