Introduction

Since Ehrlich first proposed the idea in 1909 that nascent transformed cells arise continuously in human bodies and that the immune system scans for and eradicates these transformed cells before they are manifested clinically, immune surveillance has been a controversial topic in tumor immunology (Ehrlich, 1909). In the mid-twentieth century, experimental evidence that tumors could be repressed by the immune system came from the use of tumor transplantation models. The findings from these models strongly suggested the existence of tumor-associated antigens (TAAs) that formed the basis of immune surveillance, as postulated by Burnet and Thomas (Burnet, 1957). The functional role of antigen-presenting cells (APCs) in cross-priming for T cell activation was subsequently demonstrated, and the cancer immune surveillance model was developed. However, the idea of cancer immune surveillance resisted widespread acceptance until the 1990s when experimental animal models using knockout mice validated the existence of cancer immune surveillance in chemically induced and spontaneous tumors. The central roles of immune effector cells, such as B cells, T cells, natural killer (NK) cells, and natural killer T (NKT) cells as well as type I and II interferons (IFNs) and perforin (pfp), have since been clarified in cancer immune surveillance (Dunn et al, 2002; Dunn et al., 2005).

As part of the twenty-first century concept of cancer immunoediting leading from immune surveillance to immune escape, three essential phases have been proposed (Dunn et al, 2002): (i) elimination; (ii) equilibrium; and (iii) escape. Nascent transformed cells can be eliminated initially by immune effector cells, such as NK cells, and by the secreted IFN-y in innate immune response. Elimination of transformed cells results in immune selection and immune sculpting, which induce tumor variants that decrease immunogenicity and become resistant to immune effector cells in the equilibrium phase. Eventually, during tumor progression, when the increased tumor size can be detected by imaging diagnosis, tumor-derived soluble factors (TDSFs) can induce several escape mechanisms from immune attack in the tumor microenvironment (Kim et al., 2006). This chapter provides a general overview and basic principles of immunoediting from immune surveillance to escape as well as a discussion of the central role of immune effector cells in the process of immunoedit-ing. A better understanding of the mechanisms of immunoediting during tumor progression may provide new insights for improving cancer immunotherapy.

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