Cells undergo apoptotic events during development, tissue homeostasis or disease and are subsequently cleared by phagocytes, inducing changes in the immune response. Lymphocyte apoptosis is responsible for the homeostasis of immune cells and plays an essential role in the elimination of autoreactive lymphocytes. Apoptosis also modulates neutrophil life span, regulating the balance between their function as effectors of the immune system and the clearance of potentially harmful cells. Programmed mammalian red blood cells death, or eryptosis, is a special form of apoptosis that shows all features of apoptosis, except nuclear condensation. Similarly, platelets, small, anuclear cytoplasmic fragments, develop apoptotic events that regulates platelet life span. Apoptotic events, which are enhanced in mature megakaryocytes, the platelet precursors, have been proposed as a major force driving proplatelet formation and platelet release. In addition to apoptosis, platelets undergo apoptotic-like events, including the rapid and reversible activation of caspase 3, that are essential for platelet Ca2+ signalling and aggregation independently of programmed cell death. Finally elevated apoptosis and enhanced oxidative stress in peripheral blood cells, such as platelets and lymphocytes, have been proposed as a biomarker for Alzheimer disease. This chapter describes the physiological and pathological implications of apoptosis in blood cells. © 2009 Springer Netherlands.
CITATION STYLE
Rosado, J. A. (2007). Apoptotic events in blood cells. In Apoptosis: Involvement of Oxidative Stress and Intracellular Ca2+ Homeostasi (pp. 129–149). Springer Netherlands. https://doi.org/10.1007/978-1-4020-9873-4_6
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