Immune Suppression in Head and Neck Cancers: A Review

Figure 1

Immunosuppressive mechanisms in the tumor microenvironment: several mechanisms are developed by cancerous cells to escape to the immune system such as a loss or a reduction of the expression of MHC class 1 molecules and costimulatory molecules, the expression of FasL to induce apoptosis of tumor-infiltrating lymphocytes and the production of immunosuppressive molecules such as TGF-β, PGE2, IL-6, IL-10, and adenosine. Among the subpopulations of naïve CD4⁺ T cells, CD4⁺ Th17 T cells promote inflammation by secreting IL-17 whereas CD4⁺ Th2 T cells promote antibody production by B cells. Tregs promote tumor progression by inhibiting the functions of CD4⁺ and CD8⁺ T cells and NK cells. TAMs M2 phenotype induce the expression of CD4⁺ Th2 T cell and Tregs. Moreover, M2 phenotype promote growth tumor (EGF, PDGF, TGF-β, IL-6, IL-1, and TNF-α), angiogenesis (TGF-β, VEGF, GM-CSF, TGF-α, IL-1, IL-6, and IL-8), invasion (MMPs, TNF-α, IL-1), immunosuppression (TGF-β, PGE2, and IL-10) and metastasis. MDSCs induce Treg, secrete IL-10, and inhibit CD4⁺ and CD8⁺ T cells.