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. Author manuscript; available in PMC: 2016 May 9.
Published in final edited form as: Oral Oncol. 2013 Oct 11;49(12):1089–1096. doi: 10.1016/j.oraloncology.2013.09.009

Figure 1.

Figure 1

Mechanisms of Immune Escape in HNSCC. A mechanistic understanding of HNSCC immune escape reveals potential targets for immunotherapy: (1) HNSCC tumors down-regulate antigen processing (TAP 1/2) and presentation (MHC 1). Tumors also commonly express PD-L1, the ligand for the immune checkpoint receptor PD-1. (2) The HNSCC microenvironment is characterized by an excess of immunosuppressive cytokines (e.g. TGF-β1, VEGF, IL-6 and IL-10) and a deficiency of immunostimulatory cytokines (e.g. IFN-γ). The cytokine milieu is influenced by imbalanced STAT1/STAT3 signaling. (3) Effector T cells receive negative feedback from immune checkpoints (CTLA-4, PD-1), co-inhibitory receptors which promote pathologic immune tolerance in the setting of HNSCC. Regulatory T cells also promote immune tolerance through CTLA-4 signaling. Down-regulation of NK cell receptors such as NKG2D and Fc-γ IIIa inhibits innate immune responses, including ADCC.