Cervical cancer incidence worldwide exceeds half a million new cases per year. The human papillomavirus (HPV) being the major causative agent of CC uses a variety of strategies to evade immune surveillance, where the immune status varies amongst individuals. This immune evasion altered by HPV is reflected in persistent infections, causing the evolution of cervical neoplasia. The role of the immune system in viral recognition and elimination is of extreme relevance in the development of CC. The interactions of the HLA-E ligand in the target cell along with CD94/NKG2 receptors, which are expressed predominantly, but not exclusively, on NK cells' surface, are responsible for activating or inhibiting cytotoxic activity according to their function. The engagement between HLA-E and CD94/NKG2 molecules is one of the fundamental surveillance mechanisms in patients with CIN I, II and III, where HLA-E expression increases significantly, especially in HPV 16 and 18 infections. Higher HLA-E expression was observed in most histopathological types of CC, and at the same time was correlated to best survival of the patient. This review aims to summarize and discuss the immunological role of HLA-E in the context of HPV infection and immune system evasion, and the oncogenic process of cervical cancer.

中文翻译：

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HLA-E是否可以在HPV免疫逃逸中发挥作用？

全世界每年宫颈癌的发病率超过半百万新病例。作为CC的主要病原体的人乳头瘤病毒（HPV）使用各种策略来逃避免疫监视，其中免疫状态因人而异。HPV改变的这种免疫逃逸反应反映在持续感染中，从而导致宫颈肿瘤的发展。免疫系统在病毒识别和消除中的作用与CC的发展极为相关。HLA-E配体与CD94 / NKG2受体（主要但并非唯一地在NK细胞表面表达）一起作用于靶细胞，根据其功能负责激活或抑制细胞毒性活性。HLA-E和CD94 / NKG2分子之间的结合是CIN I，II和III患者的基本监视机制之一，其中HLA-E表达显着增加，尤其是在HPV 16和18感染中。在大多数组织病理学类型的CC中观察到更高的HLA-E表达，同时与患者的最佳生存相关。这篇综述旨在总结和讨论HLA-E在HPV感染和免疫系统逃逸以及宫颈癌的致癌过程中的免疫学作用。