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. Author manuscript; available in PMC: 2015 May 26.
Published in final edited form as: J Clin Med. 2015 Mar 3;4(3):375–388. doi: 10.3390/jcm4030375

Figure 2.

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 TH1 cells in the lesion and supports regulatory T-cell differentiation from TH0 T-cells. In addition, the localized polarization of T cells toward a TH2 phenotype reduces the TH1 population in the lesion. Lack of HPV-specific TH1 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.