Schreiber, Old and Smyth 2011: cancer immunoediting
The review that set out the three Es of how the immune system shapes a cancer: elimination of many early tumours, an equilibrium in which growth is held in check, and escape when the tumour evolves ways to evade attack.
Overview
Schreiber, Old and Smyth summarised two decades of evidence, much of it from genetically modified mice, that the immune system both suppresses and sculpts tumours. In the elimination phase innate and adaptive immunity destroy many nascent cancers; in equilibrium, adaptive immunity holds surviving tumour cells dormant while editing their immunogenicity; in escape, variants that have lost antigens, upregulated PD-L1 or recruited suppressive cells grow out. The framework explained why clinically apparent cancers are poorly immunogenic and why checkpoint blockade can work.
- Immune-deficient mice develop more spontaneous and carcinogen-induced cancers, showing immune surveillance is real.
- Tumours can persist in an equilibrium state controlled by adaptive immunity, as shown by outgrowth when T cells are depleted.
- Escape occurs through loss of antigen presentation, immunosuppressive cytokines and ligands such as PD-L1, and recruitment of regulatory cells.
Immunoediting is the conceptual backbone of modern immuno-oncology: it explains tumour heterogeneity, dormancy and late relapse, and why immunotherapy works by releasing pre-existing but suppressed immunity.
- Largely based on mouse models; human equilibrium is inferred rather than observed.
- A review, so it synthesises rather than tests.
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