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Depletion of Langerhans Cells in Human Papillomavirus Type 16-Infected Skin Is Associated with E6-Mediated Down Regulation of E-Cadherin
Abstract
Human papillomavirus type 16 (HPV16) is an oncogenic virus that causes persistent infections in cervical epithelium. The chronic nature of HPV16 infections suggests that this virus actively evades the host immune response. Intraepithelial Langerhans cells (LC) are antigen-presenting cells that are critical in T-cell priming in response to viral infections of the skin. Here we show that HPV16 infection is directly associated with a reduction in the numbers of LC in infected epidermis. Adhesion between keratinocytes (KC) and LC, mediated by E-cadherin, is important in the retention of LC in the skin. Cell surface E-cadherin is reduced on HPV16-infected basal KC, and this is directly associated with the reduction in numbers of LC in infected epidermis. Expression of a single viral early protein, HPV16 E6, in KC reduces levels of cell surface E-cadherin thereby interfering with E-cadherin-mediated adhesion. Through this pathway, E6 expression in HPV16-infected KC may limit presentation of viral antigens by LC to the immune system, thus preventing the initiation of a cell-mediated immune response and promoting survival of the virus.
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“suggesting that expression of HPV oncoproteins in the infected epithelium deregulates inflammatory responses in order to sustain viral persistence.”
From The Not-So-Good, the Bad and the Ugly: HPV E5, E6 and E7 Oncoproteins in the Orchestration of Carcinogenesis (2021) · cites this paper as [370]
In the citing paper
“Furthermore, Langerhans cells, the major antigen presenting cell population of the skin, were demonstrated to be reduced in numbers in HPV-associated lesions, potentially via down regulation of E-cadherin expression mediated by E6.”
From The Not-So-Good, the Bad and the Ugly: HPV E5, E6 and E7 Oncoproteins in the Orchestration of Carcinogenesis (2021) · cites this paper as [370]
In the citing paper
“In addition, Langerhans cells were also found to be unable to initiate T-cell responses when exposed to chimeric HPV-16 virus like particles via a mechanism dependent on phosphatidylinositol kinase-3 [369,370,371,372]”
From The Not-So-Good, the Bad and the Ugly: HPV E5, E6 and E7 Oncoproteins in the Orchestration of Carcinogenesis (2021) · cites this paper as [370]
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Cited by
Molecular biology of human papillomavirus infection and cervical cancer
Doorbar, J. (2006) · Clinical Science · doi:10.1042/cs20050369 · Cited by 1,072
Self-citationCarcinogenic human papillomavirus infection
Schiffman, M., Doorbar, J., Wentzensen, N., de Sanjosé, S., Fakhry, C., Monk, B. J., Stanley, M. A., & Franceschi, S. (2016) · Nature Reviews Disease Primers · doi:10.1038/nrdp.2016.86 · Cited by 999
Self-citationBasukala, O., & Banks, L. (2021) · Viruses · doi:10.3390/v13101892 · Cited by 137
Metadata
- Authors
- Matthews, K., Leong, C. M., Baxter, L., Inglis, E., Yun, K., Bäckström, B. T., Doorbar, J., & Hibma, M.
- Affiliations
- Virus Research Unit, Department of Microbiology
- Department of Pathology
- Malaghan Institute of Medical Research, Wellington School of Medicine, University of Otago, Dunedin, New Zealand
- Virology Department, National Institute for Medical Research, London, United Kingdom
- Venue
- Journal of Virology
- Publisher
- American Society for Microbiology
- Published
- 2003-08
- Volume
- 77
- Issue
- 15
- Pages
- 8378-8385
- ISSN
- 0022-538X
- 1098-5514
- Cited by
- 125
- References
- 1
- Language
- en
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