Tumor immunology--when a cancer cell meets the immune cells.
Bor‐Ching Sheu, Su Ming Hsu, Hong‐Nerng Ho, Rong Lin, Su Huang
Abstract
Bor‐Ching Sheu, Su Ming Hsu, Hong‐Nerng Ho, Rong Lin, Su Huang
Abstract
Tumor immunology consists of two essential concepts: immune surveillance, which specifies the host immune reactions against tumor cells, and tumor immune escape, which refers to the tumor-cell evasion process against the host immune system. Effective antitumor immunity by the host immune surveillance is supposed to be dependent on the identification of tumor antigens. In the process of malignant transformation, genetic mutations with aberrant expression of cancer-related genes and protein products are potentially immunogenic, which may serve as rejection antigens. Several scenarios are proposed to be responsible for tumor immune-escape mechanisms. The elucidation of the immune deficit against cancer progression has been a difficult task and no solitary mechanism explains the complicated cancer-host immune interactions. Cancer cells may overcome immune surveillance through a common but effective pathway, either by changing the polarity of effector cells, thus down-regulating the proliferation of tumor-specific cytotoxic T cells, or altering the effector compositions of immune cells within the tumor milieu, or both. Understanding the interaction between cancer cells and host immune cells within the tumor milieu is of importance for further clinical applications of immunotherapy in cancer treatment.
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Tumor immunology consists of two essential concepts: immune surveillance, which specifies the host immune reactions against tumor cells, and tumor immune escape, which refers to the tumor-cell evasion process against the host immune system. Effective antitumor immunity by the host immune surveillance is supposed to be dependent on the identification of tumor antigens. In the process of malignant transformation, genetic mutations with aberrant expression of cancer-related genes and protein products are potentially immunogenic, which may serve as rejection antigens. Several scenarios are proposed to be responsible for tumor immune-escape mechanisms. The elucidation of the immune deficit against cancer progression has been a difficult task and no solitary mechanism explains the complicated cancer-host immune interactions. Cancer cells may overcome immune surveillance through a common but effective pathway, either by changing the polarity of effector cells, thus down-regulating the proliferation of tumor-specific cytotoxic T cells, or altering the effector compositions of immune cells within the tumor milieu, or both. Understanding the interaction between cancer cells and host immune cells within the tumor milieu is of importance for further clinical applications of immunotherapy in cancer treatment.
Key concepts: Immune system, Cancer immunotherapy, Cancer, Antigen, Immunology, Immunotherapy, Effector, Cancer cell