Figure 1.

The tumour microenvironment (TME) in head and neck cancer: Cancer-associated fibroblasts perform vital functions in angiogenesis, tumour invasion and metastasis, and inhibit T-cell function by cytokine secretion. The presence of vascular endothelial growth factor, interleukin (IL) 6 and granulocyte-macrophage colony-stimulating factor in the TME promote the aggregation of myeloid-derived suppressor cells, with the ability to suppress the activity of T cells from the production of nitric oxide by nitric oxide synthase. The presence of M2 macrophages is correlated with a worse prognosis, given their ability to release immunosuppressive cytokines and negatively regulate the activity of M1 macrophages. Effector cells and antigen presenting cells (APC) see their functions compromised from the release of immunosuppressive cytokines, B granzymes and perforins by regulatory T cells (T reg). In addition, T reg regulate the production of indoleamine-2,3-dioxygenase 1 by APC, suppressing the essential tryptophan in the proliferation of T cells, in addition to inhibiting antigenic presentation by the expression of inhibitory molecules. The presence of T and Natural Killer cells aim to exert an antitumour response; however, their function is impaired by a highly immunosuppressive TME.