Figure 2.

Innate Signaling of HPV 6/11-infected Keratinocytes Modulates the Immune Response in RRP. Keratinocytes harboring persistent HPV-infection have increased levels of PGE₂ and CCL20, while levels of the pro-inflammatory cytokine IL-36 γ are decreased. The alterations in this cytokine milieu inhibit the normal activation of Langerhans cells, which in turn reduces the number of HPV-specific T_H1 cells in the lesion and supports regulatory T-cell differentiation from T_H0 T-cells. In addition, the localized polarization of T cells toward a T_H2 phenotype reduces the T_H1 population in the lesion. Lack of HPV-specific T_H1 cells, results in low levels of HPV-specific CD8+ cells that supports a micromilieu of immune suppressive cells, chemokine, and cytokines that supports persistent HPV infection.