Alves Jayra Juliana Paiva, De Medeiros Fernandes Thales Allyrio Araújo, De Araújo Josélio Maria Galvão, Cobucci Ricardo Ney Oliveira, Lanza Daniel Carlos Ferreira, Bezerra Fabiana Lima, Andrade Vânia Sousa, Fernandes José Veríssimo
Department of Microbiology and Parasitology, Federal University of Rio Grande do Norte, Natal, RN 59072-970, Brazil.
Department of Biomedical Sciences, University of Rio Grande do Norte State, Mossoró, RN 59607-360, Brazil.
Oncol Lett. 2018 Nov;16(5):6215-6227. doi: 10.3892/ol.2018.9481. Epub 2018 Sep 21.
Persistent infection by high-risk human papillomavirus (HR-HPV) is the main risk factor for uterine cervical cancer (UCC). However, viral infection alone is not sufficient for the development and progression of premalignant cervical lesions for cancer. In previous years it has been suggested that the adaptive immune response triggered by the differentiation of naïve helper T cells in Th17 cells may serve an important role in disease development. It has been hypothesized that Th17 cells may be involved in the promotion of UCC, as high levels of interleukin 17 (IL17) expression have been detected in the mucosa of the uterine cervix of patients affected by the disease. However, the role of Th17 cells in the tumor development and progression remains unclear. It is believed that the immune response of the Th17 type during persistent infection of the genital tract with HR-HPV triggers chronic inflammation with a long duration with the production of IL17 and other pro-inflammatory cytokines, creating a favorable environment for tumor development. These cytokines are produced by immune system cells in addition to tumor cells and appear to function by modulating the host immune system, resulting in an immunosuppressive response as opposed to inducing an effective protective immune response, thus contributing to the growth and progression of the tumor. In the present review, the latest advances are presented about the function of Th17 cells and the cytokines produced by them in the development and progression of UCC.
高危型人乳头瘤病毒（HR-HPV）的持续感染是子宫颈癌（UCC）的主要危险因素。然而，仅病毒感染不足以导致癌前宫颈病变的发生和进展。近年来，有研究表明，初始辅助性T细胞分化为Th17细胞所触发的适应性免疫反应可能在疾病发展中起重要作用。据推测，Th17细胞可能参与UCC的进展，因为在该病患者的子宫颈黏膜中检测到高水平的白细胞介素17（IL17）表达。然而，Th17细胞在肿瘤发生和进展中的作用仍不清楚。据信，在HR-HPV持续感染生殖道期间，Th17型免疫反应会引发长期的慢性炎症，并产生IL17和其他促炎细胞因子，从而为肿瘤发展创造有利环境。这些细胞因子除了由肿瘤细胞产生外，还由免疫系统细胞产生，其作用似乎是调节宿主免疫系统，导致免疫抑制反应，而不是诱导有效的保护性免疫反应，从而促进肿瘤的生长和进展。在本综述中，介绍了Th17细胞及其产生的细胞因子在UCC发生和进展中的功能的最新进展。
