Immunological battlefield in gastric cancer and role of immunotherapies

Figure 1 Process of immune system killing tumour and processes of tumour evasion. A: Outlines the process of immune system killing tumour cell. First, antigens (including neo-antigens) expressed by the tumour, are recognized by immature DC then the innate immune system is activated and the antigen is presented by APC to the T cell. The T cell becomes activated, then proliferates and infiltrates into tumour sites. The adaptive immune system is then responsible for activation of the effector immune cells (e.g., CTL, Th cell or NK cell) that secrete cytokines to kill the tumour cell; B: Describes part of the processes of immune evasion. This is the mechanism by which the tumour cell evades the immune system (escape phase) through the processes of immune recognition/ignorance; immune suppression/tolerance and; adaptive immune resistance. DC: Dendritic cell; CTL: Cytotoxic T lymphocytes; Th cell: T helper cell; NK: Natural killer cell; APC: Antigen processing cell; MHC: Major histocompatibility complex; TCR: T-cell receptor.

Figure 2 Two different tumour microenvironments of different molecular subgroups of gastric cancer. A: Example of a strong immunogenic tumour with increased antigen presentation and immune checkpoints expression, more TILs and other effector immune cells infiltration into the tumour; B: Example of a weak anti-tumour immune response with less antigen expression, less TILs and other effector immune cell infiltration into tumour and increased numbers of immunosuppressive cells; C: Schematic diagram representing poor defences from a conspicuous tumour with vigorous immune response; D: Schematic diagram representing good defences from a less conspicuous tumour with minimal immune response. MDSC: Myeloid-derived suppressor cell; TAM: Tumour associate macrophages; Treg: T regulatory cell; Th17: T helper cell-17; ECM: Extracellular matrix; MHC: Major histocompatibility complex; TCR: T-cell receptor.