Published online Jan 6, 2020. doi: 10.12998/wjcc.v8.i1.11
Peer-review started: October 7, 2019
First decision: November 13, 2019
Revised: November 18, 2019
Accepted: November 30, 2019
Article in press: November 30, 2019
Published online: January 6, 2020
Processing time: 91 Days and 8.6 Hours
As one of the subsets of CD8+ T cells, Tc17 cells have recently been identified and are characterized by the secretion of interleukin (IL)-17, which is related to inflammatory diseases.
To assess the status of Tc17 cells in cervical cancer and investigate the biological function of Tc17 cells in cervical cancer development.
Flow cytometry assay, immunohistochemistry, and immunofluorescence were performed to detect the levels and phenotype of Tc17 cells in blood and tumor samples from patients with cervical cancer. Prior to cell suspension culture, ELISA was carried out to measure the production of IL-6, IL-1β, IL-23, CXCL12, and IL-17 in tumor tissue supernatant and co-cultured supernatant of patients with cervical cancer. In addition, multivariate analysis was performed to identify factors associated with overall survival using the Cox proportional hazards model.
Compared with normal tissues, Tc17 cells specifically accumulated in tumor tissues of cervical cancer patients. Cancer cells produced a greater amount of IL-6, IL-1β, and IL-23, which in turn promoted Tc17 cell polarization. Unlike the traditional cytotoxic CD8+ T cells, Tc17 cells secreted IL-17, which subsequently promoted CXCL12 expression in tumor cells, eventually enhancing the proliferation and migration of tumor cells. Thus, the ratio of tumor-infiltrating Tc17 cells was highly correlated with poor clinical outcome in patients with cervical cancer.
Our data identified the oncogenic role of Tc17 cells in the development of cervical cancer. We propose that the ratio of Tc17 cells may be a useful index in the prognosis of patients with cervical cancer.
Core tip: Inflammation contributes to cancer development. In this study, it was found that cervical cancer-elicited inflammation increased Tc17-polarizing cytokine production, which attenuated cytotoxic CD8+ T cell development. The high level of interleukin-17 production by Tc17 cells led to CXCL12 upregulation and cancer cell migration. Consistent with the oncogenic role of Tc17 cells in cancer development, the ratio of cancer-infiltrating Tc17 cells was highly associated with poor prognosis in patients with cervical cancer. Thus, our data demonstrate that Tc17 cells can be induced in cervical cancers and serve as a meaningful index in the prognosis of patients with cervical cancer.