Skip to main content
. 2021 Oct 17;13(20):5206. doi: 10.3390/cancers13205206

Figure 2.

Figure 2

A summary of immune dysregulation and evasion in the tumor microenvironment (TME) of HPV+ (left) and HPV− (right) HNSCCs. The differential immunophenotypes in the TME between HPV+ and HPV− HNSCC are depicted, based on three different spatial distribution of CD8+ T cells previously proposed [83,84]. The highly inflamed phenotype of HPV+ OPSCC may be caused by the anatomical distinction of oropharynx composed of the lymphoid tissue. CD4T, CD4+ T cell; CD8T, CD8+ T cell; Treg, regulatory T cell; B, B cell; T, T cell; M1, M1 macrophage; M2, M2 macrophage; pDC, plasmacytoid dendritic cell; HPV, HPV genome; IFN, interferon-related genes; TNFα, tumor necrosis factor-α; TGFβ, transforming growth factor-β; PD-1, programmed death-1; PD-L1, programmed death ligand-1; IL-6, interleukin 6; IL-10, interleukin 10; CXCL14, C-X-C chemokine 14.