The processes of malignancy, such as invasion and rapid growth of tumor cells, naturally cause inflammation. Dendritic cells (DCs), the most powerful antigen presenting cell (APC), should become activated to the presence of cancer cells and present sampled antigen in association with surface major histocompatibility complexes (MHC). The presentation of these tumor associated antigens (TAA), along with the appropriate costimulatory signals, leads to activation of antigen specific CD8+ T-cells. These T-cells recognize and bind that TAA on the MHC class I of tumor cells. Subsequent secretion of perforin and granzymes can induce caspase-dependent apop-tosis. However, in the many reported cases of human cancer, this process obviously does not seem to occur efficiently enough to destroy the tumor cells.
Cancer cells may evade recognition by the immune system through several mechanisms (9): (1) down-regulation of antigen processing and presentation, (2) loss of some TAA which may alert the immune system, and (3) secretion of soluble signals which can modify the ability of DCs to effectively present antigens to naïve T-cells. Examples of such secreted factors include interleukin (IL)-10, which inhibits DC maturation, and transforming growth factor (TGF)-^, which is secreted by cells in the eye to prohibit destructive inflammation (9,10). Although it is unclear to what extent these mechanisms are involved in tumor persistence, it is clear that tumor cells have developed ways to avoid immune rejection.
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