Immune deviation and cervical carcinogenesis

Abstract

Evidence is emerging that a complex interplay between high-risk human papillomavirus infection, the local microenvironment and the immune system is critical for cervical carcinogenesis. To establish persistence, the virus has to evade or overcome immune control. At the transition from precancer to cancer, however, chronic stromal inflammation and immune deviation build up, which may eventually determine the course of disease. Understanding the molecular basis underlying these pivotal stage-specific changes may help to define new tools for better diagnosis and therapy that are required to efficiently combat human papillomavirus-associated disease.