Revisiting cancer immunoediting by understanding cancer immune complexity

Abstract

Since 1909, the cancer immunosurveillance concept has undergone four distinct eras. These include a general acceptance during 1957–1974, an abandonment during 1974–1996, resurrection during 1996–2001 in the form of an elegant theory of tumour immunoediting proposed by Robert Schreiber, and a retreat since 2006. Recently, in the Journal of Pathology, Ciampricotti et al reported an elegant experimental model designed by establishing RAG2−/−/MMTV-NeuT mice. Using this, they demonstrated that the development and metastasis of HER-2/neu-positive spontaneous mammary carcinoma were not altered by the presence or absence of the adaptive immune system. Their fascinating results are a call to revisit controversial reports as to an effective role of the adaptive immune system in tumour inhibition versus tumour promotion or tolerance in the development of spontaneous carcinomas. Ciampricotti and colleagues present a strong case for revising our ideas of cancer immunoediting and appreciating the complexity of the interaction between cancer and the immune system.

Figure 1

A unified theory of cancer immune complexity. Tumours comprised of a heterogenous population of cells that expands from clones that send danger signals to the immune system (red) to clones that do not appear to be dangerous to the immune system (blue). The balance between these two clones determines the state of tumour immunosurveillance in the host. There are 10 possible pathways depicted here, which describes the interplay between tumour immunoediting and tolerance.