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上皮细胞对人乳头瘤病毒感染的免疫反应

The Epithelial Immune Response to Human Papillomavirus Infection.

作者信息

Roy-Biswas Shyantani, Hibma Merilyn

机构信息

Department of Pathology, Dunedin School of Medicine, University of Otago, P.O. Box 56, Dunedin 9054, New Zealand.

出版信息

Pathogens. 2025 May 9;14(5):464. doi: 10.3390/pathogens14050464.

Abstract

The skin is a complex organ, containing an intricate network of immune cells that are crucial for host barrier function and defence against pathogens. Human papillomavirus (HPV) exclusively infects the skin, and its lifecycle is intimately associated with epithelial cell division and differentiation. There are over 450 HPV types, 12 of which are classified as carcinogenic. The primary focus of this review is the epithelial immune response to HPV infection of the cervix during the initial stages of infection, productive infection, and disease progression. During the early stages of infection, cells are HPV-positive; however, there are no attributable histological changes to the epithelium. The HPV-infected cells have the capacity for innate sensing and signalling through toll-like receptors in response to viral nucleic acids. However, HPV has evolved multiple mechanisms to evade the innate response. During productive infection, all viral antigens are expressed and there are visible histological changes to the epithelium, including koilocytosis. Disease regression is associated with Tbet positive cells in the infected epithelium and the presence of CD4 and CD8 T cells in the lamina propria. Disease progression is associated with the overexpression of the E6 and E7 oncoproteins after integration of viral genomes into the host chromosomal DNA. Histologically, the epithelium is less differentiated, and changes to cells include a higher nuclear-to-cytoplasmic ratio and an increased mitotic index. Immune changes associated with disease progression include increased numbers of cells expressing suppressor molecules, such as FoxP3, Blimp-1, and HMGB1, and myeloid cell infiltrates with an M2-like phenotype. This review highlights the gaps in the understanding of the immune response in HPV-positive cervical neoplasia, and in regression and progression of disease. This knowledge is critical for the development of effective immunotherapies that reliably cause HPV-positive cervical neoplasia to regress.

摘要

皮肤是一个复杂的器官,包含一个错综复杂的免疫细胞网络,这些免疫细胞对于宿主屏障功能和抵御病原体至关重要。人乳头瘤病毒(HPV)专门感染皮肤,其生命周期与上皮细胞的分裂和分化密切相关。HPV有450多种类型,其中12种被归类为致癌型。本综述的主要重点是在感染初期、生产性感染和疾病进展过程中,子宫颈对HPV感染的上皮免疫反应。在感染的早期阶段,细胞呈HPV阳性;然而,上皮组织没有可归因的组织学变化。被HPV感染的细胞能够通过Toll样受体对病毒核酸进行天然感知和信号传导。然而,HPV已经进化出多种机制来逃避天然免疫反应。在生产性感染期间,所有病毒抗原都会表达,上皮组织会出现明显的组织学变化,包括空泡化细胞。疾病消退与感染上皮组织中Tbet阳性细胞以及固有层中CD4和CD8 T细胞的存在有关。疾病进展与病毒基因组整合到宿主染色体DNA后E6和E7癌蛋白的过度表达有关。在组织学上,上皮组织的分化程度较低,细胞变化包括核质比增加和有丝分裂指数增加。与疾病进展相关的免疫变化包括表达抑制分子(如FoxP3、Blimp-1和HMGB1)的细胞数量增加,以及具有M2样表型的髓样细胞浸润。本综述强调了在理解HPV阳性宫颈肿瘤形成中的免疫反应以及疾病消退和进展方面的差距。这些知识对于开发能够可靠地使HPV阳性宫颈肿瘤消退的有效免疫疗法至关重要。

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