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Cancer creates an environment of constant antigen exposure and inflammation. In this setting, T cells transform into a differentiation state that has been termed T cell exhaustion, which is characterised by upregulation of inhibitory receptors, like TIM-3 and PD-1, resulting in loss of effector function. The discovery of receptor-mediated immune checkpoints, which prevent uncontrolled T cell reactions, led to the development of a new class of antibodies termed checkpoint inhibitors, bringing exhaustion phenomena to the forefront of tumour research. Data on the efficacy of checkpoint inhibitors in pancreatic cancer are still sparse; however, preliminary results indicate limited efficacy as single agents. In order to increase therapeutic efficacy, knowledge on T cell exhaustion mechanisms in pancreatic cancer is mandatory.
Recently, sophisticated models have confirmed the notion that components of …