Figure 2.

Schematic representation of the HPV strategies likely to modify the immunological microenvironment in the site of infection. HPV has evolved mechanisms both to avoid initial recognition by the immune system as well as to interfere with adaptive immunity. A primary mechanism of viral immune evasion is likely achieved by avoiding antigen processing and presentation by Langerhans and dendritic cells (represented in the diagram as a lack of migration of these cells from the dermis). Further, HPV has evolved mechanisms capable of inhibiting key host antivirus natural and adaptive responses, including the modulation of the cascade of inflammatory or immunoregulatory cytokines and chemokines, IFN production, as well as the activity of cytotoxic T cells and natural killer cells, and the humoral antibody response. The recruitment of CD4⁺ CD25⁺ regulatory T cells (Tregs, depicted as green circles) and the presence of activated Th2 cells (depicted as red circles), can lead to a further suppression of cytotoxic functions, induction of T cell anergy, and apoptosis. The pink nuclei identify the HPV-infected epithelium. The up and down arrows represent the increased or decreased expression of cell markers or cytokines.