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Immune surveillance mechanisms represent the physiological process by which the immune system identifies and destroys abnormal cells, such as malignant or infected cells, before they develop into clinical disease (Burnet, 1970, Progress in Experimental Tumor Research). This process involves a complex interplay between innate and adaptive immunity, utilizing cells such as Natural Killer (NK) cells and CD8+ T lymphocytes to recognize tumor-associated antigens or stress signals (Dunn et al., 2002, Nature Immunology). In cancer biology, the concept has evolved into the "cancer immunoediting" hypothesis, which describes how the immune system both protects the host and shapes tumor immunogenicity through elimination, equilibrium, and escape phases (Schreiber et al., 2011, Science). Tumors often evade these mechanisms by hijacking inhibitory pathways, such as the PD-1/PD-L1 axis, to suppress immune activation (Pardoll, 2012, Nature Reviews Cancer). Therapeutic strategies like checkpoint inhibitors and CAR-T cell therapies aim to restore or enhance these surveillance mechanisms to achieve durable clinical responses. Furthermore, the clinical success of these therapies has validated the critical role of immune surveillance in controlling human malignancies (Dunn et al., 2004, Immunity). Consequently, understanding the molecular basis of immune surveillance is fundamental to the field of immuno-oncology and the development of modern biological therapies.
Restoration or enhancement of the immune system's natural ability to detect and eliminate aberrant cells by modulating immune checkpoints or enhancing antigen presentation.
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