WImmunoediting is characterized by changes in the immunogenicity of tumors due to the anti-tumor response of the immune system, resulting in the emergence of immune-resistant variants.[2]
Phase 1: Elimination[edit]
During the elimination phase, immune effector cells such as natural killer cells, with the help of dendritic and CD4+ T-cells, are able to recognize and eliminate tumor cells (left). As a result of heterogeneity, however, tumor cells which are less immunogenic are able to escape immunosurveillance (right).
The elimination phase, also known as immunosurveillance, includes innate and adaptive immune responses to tumour cells. For the innate immune response, several effector cells such as natural killer cells and T cells are activated by the inflammatory cytokines, which are released by the growing tumour cells, macrophages and stromal cells surrounding the tumour cells. The recruited NK cells macrophages produce interleukin 12 and interferon gamma, which kill tumour cells by cytotoxic mechanisms such as perforin, TNF-related apoptosis-inducing ligands (TRAILs), and reactive oxygen species.[3]
Phase 2: Equilibrium[edit]
The next step in cancer immunoediting is the equilibrium phase, during which tumor cells that have escaped the elimination phase and have a non-immmunogenic phenotype are selected for growth. It is the longest of the three processes in cancer immunoediting and may occur over a period of many years. During this period of Darwinian selection, new tumor cell variants emerge with various mutations that further increase overall resistance to immune attack.[3]
Phase 3: Escape[edit]
During the escape phase, tumor cell variants selected in the equilibrium phase have breached the host organism's immune defenses, with various genetic and epigenetic changes conferring further resistance to immune detection.
WImmunoediting is characterized by changes in the immunogenicity of tumors due to the anti-tumor response of the immune system, resulting in the emergence of immune-resistant variants.[2]Phase 1: Elimination[edit]During the elimination phase, immune effector cells such as natural killer cells, with the help of dendritic and CD4+ T-cells, are able to recognize and eliminate tumor cells (left). As a result of heterogeneity, however, tumor cells which are less immunogenic are able to escape immunosurveillance (right).The elimination phase, also known as immunosurveillance, includes innate and adaptive immune responses to tumour cells. For the innate immune response, several effector cells such as natural killer cells and T cells are activated by the inflammatory cytokines, which are released by the growing tumour cells, macrophages and stromal cells surrounding the tumour cells. The recruited NK cells macrophages produce interleukin 12 and interferon gamma, which kill tumour cells by cytotoxic mechanisms such as perforin, TNF-related apoptosis-inducing ligands (TRAILs), and reactive oxygen species.[3]Phase 2: Equilibrium[edit]The next step in cancer immunoediting is the equilibrium phase, during which tumor cells that have escaped the elimination phase and have a non-immmunogenic phenotype are selected for growth. It is the longest of the three processes in cancer immunoediting and may occur over a period of many years. During this period of Darwinian selection, new tumor cell variants emerge with various mutations that further increase overall resistance to immune attack.[3]Phase 3: Escape[edit]During the escape phase, tumor cell variants selected in the equilibrium phase have breached the host organism's immune defenses, with various genetic and epigenetic changes conferring further resistance to immune detection.
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