Elements of cancer immunity and the cancer–immune set point
Daniel S. Chen & Ira Mellman
Nature 541, 321–330 (19 January 2017) doi:10.1038/nature21349
Received 23 August 2016 Accepted 11 November 2016 Published online 18 January 2017
Immunotherapy is proving to be an effective therapeutic approach in a variety of cancers. But despite the clinical success of antibodies against the immune regulators CTLA4 and PD-L1/PD-1, only a subset of people exhibit durable responses, suggesting that a broader view of cancer immunity is required. Immunity is influenced by a complex set of tumour, host and environmental factors that govern the strength and timing of the anticancer response. Clinical studies are beginning to define these factors as immune profiles that can predict responses to immunotherapy. In the context of the cancer-immunity cycle, such factors combine to represent the inherent immunological status — or 'cancer–immune set point' — of an individual.
Figure 5: Factors that influence the cancer–immune set point
A map of cancer immunity showing the factors that affect the cancer–immune set point. The factors are placed on rings that denote their type, and each factor is also placed in the step of the cancer-immunity cycle in which they mainly act. For example, variations in HLA type reflect host genetics and are of greatest importance for T cell activation. Additional factors are being discovered rapidly. ARNTL, aryl hydrocarbon receptor nuclear translocator–like protein 1; ATG16L, autophagy-related protein 16; FcγRIII, Fc γ receptor III; HMGCR, HMG-CoA reductase; JAK/STAT, Janus kinase–signal transducers and activators of transcription; LOX, lysyl oxidase; NOD, nucleotide-binding oligomerization domain-containing protein; NSAIDs, non-steroidal anti-inflammatory drugs; RANKL; receptor activator of NF-κB ligand; ROS, reactive oxygen species.
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