Abstract

Ramya Balaprabha G.*, Sucheta Krupalani Chinnam, Sravani Datta Kandala and Shiva Chandra Madapati

ABSTRACT

Cervical intraepithelial neoplasia (CIN) and cervical cancer are primarily attributed to human papillomavirus (HPV) infection. The virus can remain undetected for extended durations due to its ability to evade the immune system and disrupt normal cell cycle regulation through its integration into host cells. Following HPV infection, the host's immune system may develop a state of immunotolerance, which affects the maturation and function of various immune cells, including regulatory T cells, dendritic cells, natural killer cells, CD4+/CD8+ T cells, and macrophages. This immunological alteration encompasses the differentiation of tumorassociated macrophages, a compromised cellular immune response, an imbalance between Th1 and Th2 cells, infiltration of regulatory T cells, and a reduction in the activation and maturation of dendritic cells. In response to these immune changes, therapeutic vaccines aimed at activating the immune response are becoming increasingly prominent for the treatment of HPVrelated conditions, alongside the development of preventive vaccines designed to mitigate the risk of carcinogenesis. Evidence suggests a correlation between T cell infiltration and the regression of disease. In studies involving animal models, especially rabbits and canines, there is a significant elevation of CD11c, CD4, and CD8+ T cells observed during the early stages of regression and adaptive immune responses.