Abstract
The interplay between cervical cancer (CC) and immune cells, mainly intratumoral lymphocytes, has a pivotal role in carcinogenesis. In this context, we evaluated the distribution of CD45RA+ and CD45RO+ cells as well as CCR6+ and CCL20+ cells in intraepithelial (IE) and marginal stroma (MS) areas from cervical intraepithelial neoplasia (CIN) I–III, and CC as ‘immunoscore’ for HPV-induced CC outcome. We observed increased CD45RA+ and CD45RO+ cells distribution in IE and MS areas in the CC group compared to CIN groups and healthy volunteers. Interestingly, there is a remarkable reduction of CCL20+ expressing cells distribution according to lesion severity. The CC group had a significant decrease in CCL20+ and CCR6+-expressing cells distribution in both IE and MS areas compared to all groups. Using the ‘immunoscore’ model, we observed an increased number of women presenting high CD45RA+/CD45RO+ and low CCL20+/CCR6+ ‘immunoscore’ in the CC group. Our results suggested a pattern in cervical inflammatory process with increasing CD45RA+/CD45RO+, and decreasing CCL20+/CCR6+ expression in accordance with CIN severity. Taken together, these markers could be evaluated as ‘immunoscore’ predictors to CC response. A more comprehensive analysis of longitudinal studies should be conducted to associate CD45RA+/CD45RO+ and CCL20+/CCR6+ ‘immunoscore’ to CC progression and validate its value as a prognosis method.
Highlights
Despite advances in prevention and early detection, cervical cancer (CC) is the fourth most common type of cancer in the female population w orldwide[1] and is associated with the human papillomavirus (HPV) infection in 99.7% of CC cases[2]
We investigated the possible correlation between intralesional immune cell profile and HPV-associated cervical lesion severity
We identified the CD45RA+, CD45RO+, CCL20+ and C CR6+ expressing cell distribution in cervical lesions and CC
Summary
Despite advances in prevention and early detection, cervical cancer (CC) is the fourth most common type of cancer in the female population w orldwide[1] and is associated with the human papillomavirus (HPV) infection in 99.7% of CC cases[2]. Some studies have evaluated how tumor-infiltrating immune cells (TICs) interact with cancer cells, shape the TME and affect clinical outcomes[14]. New methods based on the density of lymphocyte populations have been established to predict the outcome of colon c ancer[20,21,22] This method, known as ‘immunoscore’ incorporated the number, type, and distribution of immune cells in cancer tissue. In cervical lesions, it may be applied in the CIN-II diagnosis, through the identification of Ki67 and p16 b iomarkers[23] or in study of tumor-induced immune suppression and escape, mediated by the programmed cell death receptor 1 (PD-1) and its ligand (PD-L1)[24]
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