Abstract:

The incidence of cervical cancer ranks first in gynecological malignancies. Human papilloma virus (HPV) infection is a prerequisite for the occurrence of cervical cancer. Among them, persistent infection of high-risk HPV greatly increases the risk of cervical cancer. After HPV infection, its DNA is integrated into the host cell DNA, and the integration process will lead to the deletion of many early and late genes encoded by the virus, which further leads to the uncontrolled host cell cycle, resulting in cervical lesions. At the same time, HPV changes the immune microenvironment of the cervix through a variety of ways, which leads to the decline of the body′s local immune function, which in turn leads to immune escape and promotes disease progression. During this period, not only experienced the innate immune process involving macrophages, natural killer cells and dendritic cells, but also experienced the adaptive immune response dominated by T cells. The above-mentioned various immune cells and their secreted cytokines interact and cooperate with each other, and together play an important role in cervical cancer immune escape and tumor immune response. Clarifying the relationship between HPV infection, immune cells, immune factors and immune escape will provide directions for cervical cancer treatment.

Key words: Uterine cervical neoplasms, Papillomaviridae, Macrophages, Killer cells,natural, Dendritic cells, T-lymphocytes