[HTML][HTML] Apoptosis by death factor

S Nagata - cell, 1997 - cell.com
cell, 1997cell.com
There is an old Japanese saying that “Once we are in the land of the living, we will
eventually die.” This is true, not only for human beings, but also for the cells that constitute
our bodies. By repeated cell division (mitosis) and differentiation, a fertilized egg produces
billions of cells to create our bodies. During this process, many surplus or harmful cells are
generated, and they must be removed or killed (Jacobson et al., 1997 [this issue of Cell]. For
example, thymocytes that have failed to rearrange their T cell–receptor gene, or whose T cell …
There is an old Japanese saying that “Once we are in the land of the living, we will eventually die.” This is true, not only for human beings, but also for the cells that constitute our bodies. By repeated cell division (mitosis) and differentiation, a fertilized egg produces billions of cells to create our bodies. During this process, many surplus or harmful cells are generated, and they must be removed or killed (Jacobson et al., 1997 [this issue of Cell]. For example, thymocytes that have failed to rearrange their T cell–receptor gene, or whose T cell receptor may recognize their own tissues, must be eliminated. The magnitude of the cell death is staggering: more than 95% of thymocytes die in the thymus during maturation. Even in adults, senescent cells are removed and replaced by newly generated cells to maintain homeostasis. The cell death that occurs during embryogenesis, metamorphosis, endocrine-dependent tissue atrophy, and normal tissue turnover is “programmed cell death,” mediated by a process termed “apoptosis.”
Here, I focus on apoptosis controlled by cytokines. Two death factors, Fas ligand (FasL) or tumor necrosis factor (TNF), bind to their receptors and induce apoptosis, killing the cells within hours. In a classic definition of apoptosis, cells die by “suicide;” that is, cells programmed to die would do so autonomously. However, the identification of death factor–receptor pairs that regulate apoptosis indicates that apoptosis can also be controlled by an external killer in some instances.
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