Bcl-2 and Bcl-2-Related Proteins in Apoptosis Regulation

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Abstract
Apoptosis is a form of cell death critical for the normal development of multicellular organisms (Kerr et al. 1972; Wyllie et al. 1980). It is characterized by morphological and biochemical criteria consisting of: nuclear shrinkage, chromatin condensation, cytoplasmic blebbing, and internucleosomal DNA fragmentation (Kerr et al. 1972; Wyllie et al. 1980; Cohen and Duke 1992). As opposed to other forms of cell death, apoptosis does not induce an inflammatory response. There are a number of ways by which cell death by apoptosis can be induced, including growth factor deprivation, cytokine treatment, antigen-receptor engagement, cell-cell interactions, irradiation, and glucocorticoids (Cohen and Duke 1992). Within the immune system, the regulation of cell death appears to be crucial for the prevention of autoimmune disease. Immature lymphocytes are particularly susceptible to apoptosis, as 95% of thymocytes die in situ during development. Self-reactive lymphocytes are eliminated from the immune repertoire following engagement of their antigen-specific receptors. Thus, the process of clonal deletion by apoptosis allows for the elimination of self-reactive lymphocytes without initiating an inflammatory response.

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