8536d_ch02_024-0569/6/02 9: 00 PM Page 28 macas Mac 85: 365_smm pldsby et al./ Immunology Se mema su stem popuauons, Incuding those of tne leasing t creseosand possiBly triggering a damaging in Cells undergoing programmed cell death often exhibit Each of the leukocytes produced by hematopoiesis has distinctive morphologic changes, collectively referred to characteristic life span and then dies by programmed ce as apoptosis(Figures 2-3, 2-4). These changes include a death. In the adult human, for example, there are about pronounced decrease in cell volume, modification of the cy- 5 X 10 neutrophils in the circulation. These cells have a toskeleton that results in membrane blebbing, a condensa- life span of only a few days before programmed cell death tion of the chromatin, and degradation of the DNA into is initiated. This death, along with constant neutrophil smaller fragments. Following these morphologic changes, an production, maintains a stable number of these cells. If apoptotic cell sheds tiny membrane-bounded apoptotic bod- programmed cell death fails to occur, a leukemic state may s containing intact organelles. Macrophages quickly phago- develop Programmed cell death also plays a role in main cytose apoptotic bodies and cells in the advanced stages of taining proper numbers of hematopoietic progenitor cell apoptosis. This ensures that their intracellular contents, in- For example, when colony-stimulating factors are re- cluding proteolytic and other lytic enzymes, cationic pro- moved, progenitor cells undergo apoptosis. Beyond teins, and oxidizing molecules are not released into the hematopoiesis, apoptosis is important in such immuno- urrounding tissue. In this way, apoptosis does not induce a logical processes as tolerance and the killing of target cells local inflammatory response. Apoptosis differs markedly by cytotoxic T cells or natural killer cells. Details of th from necrosis, the changes associated with cell death arising mechanisms underlying apoptosis are emerging; Chapte from injury. In necrosis the injured cell swells and bursts, re- 13 describes them in detail NECROSIS APOPTOSIS Chromatin clumping Mild convolution tion Flocculent mitochondria nd segregation Condensation Blebbing Apoptotic Disintegration Phagocytosis Release of intracellular Phagocytic nflammation FIGURE 2-3 Comparison of morphologic changes that occur in tory response. In contrast, necrosis, the process that leads to death poptosis and necrosis. Apoptosis, which results in the programmed of injured cells, results in release of the cells'contents, which may in- ell death of hematopoietic cells, does not induce a local inflamma- duce a local inflammatory response Gotowww.whfreeman.com/immun② Cell Death28 PART I Introduction many types of cell populations, including those of the hematopoietic system. Cells undergoing programmed cell death often exhibit distinctive morphologic changes, collectively referred to as apoptosis (Figures 2-3, 2-4). These changes include a pronounced decrease in cell volume, modification of the cy￾toskeleton that results in membrane blebbing, a condensa￾tion of the chromatin, and degradation of the DNA into smaller fragments. Following these morphologic changes, an apoptotic cell sheds tiny membrane-bounded apoptotic bod￾ies containing intact organelles. Macrophages quickly phago￾cytose apoptotic bodies and cells in the advanced stages of apoptosis. This ensures that their intracellular contents, in￾cluding proteolytic and other lytic enzymes, cationic pro￾teins, and oxidizing molecules are not released into the surrounding tissue. In this way, apoptosis does not induce a local inflammatory response. Apoptosis differs markedly from necrosis, the changes associated with cell death arising from injury. In necrosis the injured cell swells and bursts, re￾leasing its contents and possibly triggering a damaging in￾flammatory response. Each of the leukocytes produced by hematopoiesis has a characteristic life span and then dies by programmed cell death. In the adult human, for example, there are about 5 1010 neutrophils in the circulation. These cells have a life span of only a few days before programmed cell death is initiated. This death, along with constant neutrophil production, maintains a stable number of these cells. If programmed cell death fails to occur, a leukemic state may develop. Programmed cell death also plays a role in main￾taining proper numbers of hematopoietic progenitor cells. For example, when colony-stimulating factors are re￾moved, progenitor cells undergo apoptosis. Beyond hematopoiesis, apoptosis is important in such immuno￾logical processes as tolerance and the killing of target cells by cytotoxic T cells or natural killer cells. Details of the mechanisms underlying apoptosis are emerging; Chapter 13 describes them in detail. NECROSIS APOPTOSIS Chromatin clumping Swollen organelles Flocculent mitochondria Mild convolution Chromatin compaction and segregation Condensation of cytoplasm Nuclear fragmentation Blebbing Apoptotic bodies Phagocytosis Phagocytic cell Apoptotic body Disintegration Release of intracellular contents Inflammation FIGURE 2-3 Comparison of morphologic changes that occur in apoptosis and necrosis. Apoptosis, which results in the programmed cell death of hematopoietic cells, does not induce a local inflamma￾tory response. In contrast, necrosis, the process that leads to death of injured cells, results in release of the cells’ contents, which may in￾duce a local inflammatory response. Go to www.whfreeman.com/immunology Animation Cell Death 8536d_ch02_024-056 9/6/02 9:00 PM Page 28 mac85 Mac 85:365_smm:Goldsby et al. / Immunology 5e: