The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
Human Papillomavirus Can Escape Immune Recognition through Langerhans Cell Phosphoinositide 3-Kinase Activation
Abstract
Human papillomavirus (HPV) infection of cervical epithelium is linked to the generation of cervical cancer. Although most women infected with HPV clear their lesions, the long latency period from infection to resolution indicates that HPV evolved immune escape mechanisms. Dendritic cells, which are targeted by vaccination procedures, incubated with HPV virus-like particles induce an HPV-specific immune response. Langerhans cells (LC), which are located at the sites of primary infection, do not induce a response implicating the targeting of LC as an immune escape mechanism used by HPV. LC incubated with HPV virus-like particles up-regulate the phosphoinositide 3-kinase (PI3-K) pathway and down-regulate MAPK pathways. With the inhibition of PI3-K and incubation with HPV virus-like particles, LC initiate a potent HPV-specific response. PI3-K activation in LC defines a novel escape mechanism used by HPV, and PI3-K inhibition may serve as an effective clinical target to enhance HPV immunity.
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“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 [372]
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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 [372]
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 [372]
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Guha, M., & Mackman, N. (2002) · Journal of Biological Chemistry · doi:10.1074/jbc.m203298200 · Cited by 799
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Cited by
Basukala, O., & Banks, L. (2021) · Viruses · doi:10.3390/v13101892 · Cited by 137
Candida albicans mannoprotein influences the biological function of dendritic cells
Pietrella, D., Bistoni, G., Corbucci, C., Perito, S., & Vecchiarelli, A. (2006) · Cellular Microbiology · doi:10.1111/j.1462-5822.2005.00651.x · Cited by 75
Metadata
- Authors
- Fausch, S. C., Fahey, L. M., Da Silva, D. M., & Kast, W. M.
- Affiliations
- Norris Comprehensive Cancer Center, University of Southern California , Los Angeles, CA 90089
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2005-06-01
- Volume
- 174
- Issue
- 11
- Pages
- 7172-7178
- ISSN
- 0022-1767
- 1550-6606
- Cited by
- 60
- References
- 1
- Language
- en
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- CoChat. (2026). Citation check: Human Papillomavirus Can Escape Immune Recognition through Langerhans Cell Phosphoinositide 3-Kinase Activation. https://app.cochat.ai/papers/10.4049/jimmunol.174.11.7172
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- Fausch, S. C., Fahey, L. M., Da Silva, D. M., & Kast, W. M. (2005). Human Papillomavirus Can Escape Immune Recognition through Langerhans Cell Phosphoinositide 3-Kinase Activation. The Journal of Immunology. https://doi.org/10.4049/jimmunol.174.11.7172
