We present a mathematical model to investigate the role of the immune response in controlling tumor growth in situ on cervical cells, focusing on pre-neoplastic lesions resulting from high-risk human papillomavirus infection. Our model captures the complex interplay between antigen-presenting cells and cytotoxic T-lymphocytes, which are critical components of the immune response against cancer. Through sensitivity and bifurcation analyses, we identify key parameters that generate variability and could trigger bifurcations in the system equations, providing insights into the underlying causes of disease progression. Our parameterization enables us to reproduce scenarios of elimination, recurrence, latency, and invasion of precancerous lesions, and we analyzed the events contributing to cervical intraepithelial neoplasia recurrence in women. Our findings underscore the crucial role of the immune response in controlling disease progression in the avascular stage and highlight the importance of identifying pathogenic antigens emitted by precancerous cells and the virus to achieve effective protection against cervical cancer cell growth. Overall, our study identifies key parameters of the immune response that, if improved, could promote the elimination of cervical cancer, providing a valuable starting point for future research aimed at preventing cervical cancer.