Prognostic impact of anticancer immune responses: an introduction

Abstract

Cancer cells escape innate and adaptive immune responses by selection of non-immunogenic tumor cell variants (immunoediting) or by active suppression of the immune response (immunosubversion). One common strategy that employs tumor cells to elude a T-cell-mediated immune response is the downregulation or loss of expression of HLA class I molecules, often associated with an induction of the surface expression of HLA class II antigen, nonclassical HLA class I molecules, and/or NK cell-activating ligands such as MICA, MICB, or ULBP. These changes in the surface characteristics of tumor cells result from the selection pressure exerted by immune cells from the innate and adaptive compartment. The tumor antigen characteristics are “immunoedited” in the course of the disease, resulting in the survival of tumor variants with defective antigen presentation, mostly at the level of HLA class I.