| Summary: | 5 SUMMARY Anticancer immunity is a complex network in which innate immunity play an critical role. The immune system can control the onset of tumors by recognizing the changed phenotype of the transformed cells as a non-self phenotype. The active control against cells not presenting self characters is defined by the paradigm of immune surveillance. In recent years, various studies have shown that the immune response against transformed cells start as a localized acute inflammatory response. The cooperation of natural-killer cells (NK) and phagocytes attracted by so-called "danger signals" (pro-inflammatory molecules and chemo-attractants delivered by stressed cells) can lead to total ablation of the harmful cell clone. If the intervention is not completely efficient, immunoediting of the tumor can follow with stimulation of chronic inflammatory responses, mainly mediated by macrophages. The systemic immunity attempt to terminate the uncontrolled inflammation stimulates the intervention of regulatory T lymphocytes and the shift from an antitumor cytotoxic Th1 response to a Th2 inhibitory response. This regulatory mechanism paradoxically assists the tumor development. All the described events needs the interplay and cooperation of both tumor cells and host cells and stromal elements, that altogether form the...
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