生物
免疫系统
趋化因子
基因型
细胞因子
人乳头瘤病毒
机制(生物学)
免疫学
细胞生物学
病毒学
癌症研究
基因
遗传学
内科学
医学
认识论
哲学
作者
Diane M. Da Silva,Carly Anne Movius,Adam B. Raff,Heike E. Brand,Joseph G. Skeate,Michael K. Wong,W. Martin Kast
出处
期刊:Virology
[Elsevier]
日期:2014-03-01
卷期号:452-453: 279-286
被引量:27
标识
DOI:10.1016/j.virol.2014.01.031
摘要
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.
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