Cervical cancer is the fourth most common cancer worldwide, and it is associated with human papillomavirus (HPV) infection. In general, most of cervical lesions regress spontaneously, indicating that HPV infection is not sufficient for inducing carcinogenesis. The immune system has a crucial role in HPV infection control, however there is still much to be investigated. Thus, this study aimed to identify the presence of Langerhans cells (LC, CD1a+) and activated T lymphocytes, induced by HPV-infection. The study enrolled 68 women, aged from 18 to 50 years old. From these, 17 were volunteers without cervical lesion, and 51 presenting HPV-related cervical intraepithelial neoplasia (CIN I-III, n=17 in each group). HPV-DNA was observed in 46 (90.2%) of 51 CIN volunteers, and all of women from the control group were HPV-negative. We observed an increase of CD45RA+ (naives) cells and CD45RO+ (activated, memory) cells distribution in the epithelium and basal layer of high-grade lesions (CIN II and/or CIN III) when compared with the control group. In relation to LC, our study showed a reduced number of these cells in low-grade lesions in all of investigated areas when compared with the control group, according to pre-malign lesions evolution. For CCL20 analysis, we observed an increased number of these chemokine-expressing cells in the stroma area, in relation to lesions severity. On the other hand, we observed a decrease of these cells in the epithelium. An increase of the distribution of CCR6+ (CCL20 receptor) cells in the basal layer of the epithelium in high-grade lesions (CIN II and III) occurred when compared with the control group. Thus, we concluded that LC and T lymphocytes migrate in direction to the epithelium area, where viral infection occurs, in association with the different cervical lesions degree. However, the inflammatory cells bordering the epithelial areas, focusing the stroma area, indicate that HPV can influence the lesions microenvironment, changing negatively the inflammatory cells recruitment to the site of infection.
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