Cancer Immunotherapy: Targeting Checkpoint Blockade

Abstract

Immune system is developed in such a way that it can efficiently recognize, target and eliminate foreign pathogens effectively, but leave the host self-architecture intact. During the developmental process self-reactive high avidity immune effectors are deleted, and several other mechanisms are put in place to ensure that the self-reactive low avidity immune effectors cannot generate harmful autoimmune reactions. T cells are critical immune effectors of a protective antigen specific adaptive immune response. While engagement of the T cell receptor (TCR) critical for the development of antigen specific T cell response, development of effector function in T cells is fine tuned by positive factors, the co-stimulatory factors, and negative factors, the co-inhibitory receptors. While role of co- stimulation was initially considered critical for the generation of an optimum protective immune response, it is well established that the co-inhibitory molecules play equally essential role in this process. Approaches targeting co- inhibitory receptor mediated immune blockade mechanisms have recently been shown to produce remarkable protective responses in cancer patients. We will here take a brief account of the recent advances towards development of immune checkpoint blockade strategies in cancer immunotherapy.