A Major Role for the Minor Capsid Protein of Human Papillomavirus Type 16 in Immune Escape
A Major Role for the Minor Capsid Protein of Human Papillomavirus Type 16 in Immune Escape
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DOI：
10.4049/jimmunol.0902145
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发表时间：
2009-11-15
影响因子：
4.4
通讯作者：
Kast, W. Martin
中科院分区：
文献类型：
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作者：
Fahey, Laura M.;Raff, Adam B.;Kast, W. Martin
宫颈上皮的高危人乳头瘤病毒(HPV)感染与宫颈癌的发生有因果关系。HPV不会激活感染部位的朗格汉斯细胞(LC)，导致免疫逃避。导致这种免疫逃逸的HPV蛋白尚未确定。我们证明，暴露于HPV16L1L2病毒样颗粒中的次要衣壳蛋白L2的LC不会在表型或功能上成熟。然而，HPV16L1病毒样颗粒可显著诱导LC活化。我们的数据表明，L2蛋白在通过操纵LC诱导HPV16的免疫逃逸中起着特定的作用。这一新的功能是第一次归因于L2蛋白的免疫调节作用，并大大加深了我们对HPV免疫逃逸机制的理解。免疫学杂志，2009,183：6151-6156。
High-risk human papillomavirus (HPV) infection of the cervical epithelium is causally linked with the generation of cervical cancer. HPV does not activate Langerhans cells (LC), the APC at the site of infection, leading to immune evasion. The HPV protein responsible for inducing this immune escape has not been determined. We demonstrate that LC exposed to the minor capsid protein L2 in HPV16L1L2 virus-like particles do not phenotypically or functionally mature. However, HPV16L1 virus-like particles significantly induce activation of LC. Our data suggest that the L2 protein plays a specific role in the induction of this immune escape of HPV16 through the manipulation of LC. This novel function is the first immune modulating action attributed to the L2 protein and adds significantly to our understanding of the mechanism of HPV immune escape. The Journal of Immunology, 2009, 183: 6151-6156.