The debate has been raging for many years about the immune system’s
ability to identify and destroy emerging tumor cells, and to thereby act as a barrier to
cancer development. Investigators have now used both murine models and human
studies to offer convincing evidence in support of this concept. Accumulating
information about the particular effector molecules and immune cell types involved in
this process has formed the basis for rational design of immunotherapies. Both T
lymphocytes and Natural killer (NK) cells participate in cancer immune surveillance.
Intricate effector mechanisms are involved in providing protection against both
malignant and virally infected cells. Our vision of NK cells as therapeutic agents has
evolved from the seminal discovery of inhibitory and activating NK receptors. NK cells
can recognize tumor cells while preserving normal self, and the understanding of the
mechanisms allowing for this preferential recognition pattern has greatly impacted the
success of stem cell therapy and immunotherapy. Two main strategies are used by NK
cells to recognize tumor targets. A number of tumor cells down-regulate major
histocompatibility complex (MHC) class I molecules, protecting against T-cell
recognition but releasing the inhibitory breaks in NK cells. The balance of activating
and inhibitory NK receptor signals determines whether nascent tumor cells will be
recognized and destroyed. In this chapter, the concepts of immune surveillance,
immunoediting and NK immunotherapy are discussed. Effective NK immunotherapy
may become a reality for many types of cancers in the near future.
Keywords: Activation-dependent cellular cytotoxicity, adaptor molecules, adoptive
cell therapy, apoptosis, cancer, cytokines, cytotoxicity, immune surveillance,
immunoediting, immunotherapy, interferon, interleukin, lymphocyte, killer
immunoglobulin-like receptor, major histocompatibility complex, natural killer cell,
natural killer cell receptor, signaling, stem cell transplantation, tumor necrosis factor.
