慢性人乳头瘤病毒感染期间抗原呈递细胞功能的调节
Modulation of antigen presenting cell functions during chronic HPV infection.
作者信息
Bashaw Abate Assefa, Leggatt Graham R, Chandra Janin, Tuong Zewen K, Frazer Ian H
机构信息
The University of Queensland Diamantina Institute, Translational Research Institute, Princess Alexandra Hospital, 37 Kent Street, Woolloongabba, Queensland 4102, Australia.
The University of Queensland Diamantina Institute, Translational Research Institute, Princess Alexandra Hospital, 37 Kent Street, Woolloongabba, Queensland 4102, Australia.
出版信息
Papillomavirus Res. 2017 Dec;4:58-65. doi: 10.1016/j.pvr.2017.08.002. Epub 2017 Aug 18.
High-risk human papillomaviruses (HR-HPV) infect basal keratinocytes, where in some individuals they evade host immune responses and persist. Persistent HR-HPV infection of the cervix causes precancerous neoplasia that can eventuate in cervical cancer. Dendritic cells (DCs) are efficient in priming/cross-priming antigen-specific T cells and generating antiviral and antitumor cytotoxic CD8+ T cells. However, HR-HPV have adopted various immunosuppressive strategies, with modulation of DC function crucial to escape from the host adaptive immune response. HPV E6 and E7 oncoproteins alter recruitment and localization of epidermal DCs, while soluble regulatory factors derived from HPV-induced hyperplastic epithelium change DC development and influence initiation of specific cellular immune responses. This review focuses on current evidence for HR-HPV manipulation of antigen presentation in dendritic cells and escape from host immunity.
高危型人乳头瘤病毒（HR-HPV）感染基底角质形成细胞，在某些个体中，它们能逃避宿主免疫反应并持续存在。子宫颈的持续性HR-HPV感染会导致癌前瘤形成，最终可能发展为宫颈癌。树突状细胞（DC）能有效地启动/交叉启动抗原特异性T细胞，并产生抗病毒和抗肿瘤的细胞毒性CD8+T细胞。然而，HR-HPV采取了多种免疫抑制策略，其中DC功能的调节对于逃避宿主适应性免疫反应至关重要。HPV E6和E7癌蛋白会改变表皮DC的募集和定位，而HPV诱导的增生上皮产生的可溶性调节因子会改变DC的发育，并影响特异性细胞免疫反应的启动。本综述重点关注HR-HPV操纵树突状细胞抗原呈递并逃避宿主免疫的现有证据。
Zotero 插件