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人乳头瘤病毒16型E5癌蛋白:免疫逃逸及相关免疫疗法

hrHPV E5 oncoprotein: immune evasion and related immunotherapies.

作者信息

de Freitas Antonio Carlos, de Oliveira Talita Helena Araújo, Barros Marconi Rego, Venuti Aldo

机构信息

Department of Genetics, Laboratory of Molecular Studies and Experimental Therapy (LEMTE), Center of Biological Sciences, Federal University of Pernambuco, Av. Prof Moraes Rego, 1235, Cidade Universitária, Recife, CEP 50670-901, Brazil.

Department of Research, HPV-Unit, UOSD Tumor Immunology and Immunotherapy Unit, Advanced Diagnostic and Technological Innovation, Regina Elena National Cancer Institute, Via Elio Chianesi 53, 00144, Rome, Italy.

出版信息

J Exp Clin Cancer Res. 2017 May 25;36(1):71. doi: 10.1186/s13046-017-0541-1.

Abstract

The immune response is a key factor in the fight against HPV infection and related cancers, and thus, HPV is able to promote immune evasion through the expression of oncogenes. In particular, the E5 oncogene is responsible for modulation of several immune mechanisms, including antigen presentation and inflammatory pathways. Moreover, E5 was suggested as a promising therapeutic target, since there is still no effective medical therapy for the treatment of HPV-related pre-neoplasia and cancer. Indeed, several studies have shown good prospective for E5 immunotherapy, suggesting that it could be applied for the treatment of pre-cancerous lesions. Thus, insofar as the majority of cervical, oropharyngeal and anal cancers are caused by high-risk HPV (hrHPV), mainly by HPV16, the aim of this review is to discuss the immune pathways interfered by E5 oncoprotein of hrHPV highlighting the various aspects of the potential immunotherapeutic approaches.

摘要

免疫反应是对抗人乳头瘤病毒(HPV)感染及相关癌症的关键因素,因此,HPV能够通过癌基因的表达促进免疫逃逸。特别是E5癌基因负责调节多种免疫机制,包括抗原呈递和炎症途径。此外,E5被认为是一个有前景的治疗靶点,因为目前仍没有有效的药物疗法来治疗HPV相关的癌前病变和癌症。事实上,多项研究已显示E5免疫疗法具有良好的前景,表明其可用于治疗癌前病变。因此,鉴于大多数宫颈癌、口咽癌和肛门癌是由高危型HPV(hrHPV)引起的,主要是HPV16,本综述的目的是讨论hrHPV的E5癌蛋白干扰的免疫途径,突出潜在免疫治疗方法的各个方面。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/219b/5445378/a8616657fd17/13046_2017_541_Fig1_HTML.jpg

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