Immune checkpoint inhibitors: In order for an immune response to be productive, the approval of multiple immunological checkpoints is required. These checkpoints tend to include inhibitory pathways programmed to minimise autoimmunity (damage to normal cells and tissues via one’s own immune response). Although it is apparent that the functions of immune-checkpoints are necessary, it is known that tumours use such pathways as a mechanism of immune evasion (Korman, Peggs and Allison, 2006). Considering most immune checkpoints involve ligand-receptor relations (Pardoll, 2012), they can easily be blocked by antibodies or replaced by recombinant ligands or receptors. Blockages reduce self-tolerance allowing the identification and destruction of neoplastic cells. Examples, of cancer treatments involving immune checkpoint inhibition include the blockage of CTLA-4 (a cytotoxic T-lymphocyte associated protein) or of PD-1 (a programmed cell death protein, also found on T cells). …show more content…
CTLA-4 works to down-regulate T-cell function by preventing co-stimulation of receptor CD28 and its ligand B7 (Linsley, 1991). Blocking of CTLA-4 was first introduced in advanced melanoma patients, using the drug ipilimumab (Ott, 2014). Statistics released in 2010, show that ipilimumab has been successful at prolonging the life of patients with metastatic melanoma (Couzin-Frankel, 2013). Trial participants lived an average of ten months on the antibody, whilst those without it lived only six. Despite, such promising results and approval from the Food and Drug Administration (Mulcahy, 2011), it seems that the use of ipilimumab doesn’t come without side effects. Fellner (2012) states that 80% of patients treated with ipilimumab show adverse side effects, including immune-mediated enterocolitis, hepatitis, dermatitis and