| Literature DB >> 24606705 |
Diane M Da Silva1, Carly A Movius2, Adam B Raff3, Heike E Brand3, Joseph G Skeate2, Michael K Wong4, W Martin Kast5.
Abstract
Human papillomavirus (HPV) has evolved mechanisms that allow it to evade the human immune system. Studies have shown HPV-mediated suppression of activation of Langerhans cells (LC) is a key mechanism through which HPV16 evades initial immune surveillance. However, it has not been established whether high- and low-risk mucosal and cutaneous HPV genotypes share a common mechanism of immune suppression. Here, we demonstrate that LC exposed to capsids of HPV types 18, 31, 45, 11, (alpha-papillomaviruses) and HPV5 (beta-papillomavirus) similarly suppress LC activation, including lack of costimulatory molecule expression, lack of cytokine and chemokine secretion, lack of migration, and deregulated cellular signaling. In contrast, HPV1 (mu-papillomavirus) induced costimulatory molecule and cytokine upregulation, but LC migration and cellular signaling was suppressed. These results suggest that alpha and beta HPV genotypes, and partially a mu genotype, share a conserved mechanism of immune escape that enables these viruses to remain undetected in the absence of other inflammatory events.Entities:
Keywords: Antigen presentation; Antigen presenting cell; Human papillomavirus; Immune escape; Immune suppression; Langerhans cell; Migration
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Year: 2014 PMID: 24606705 PMCID: PMC3987942 DOI: 10.1016/j.virol.2014.01.031
Source DB: PubMed Journal: Virology ISSN: 0042-6822 Impact factor: 3.616