Apoptosis (programmed cell death) is the physiological way of the elimination of unnecessary cells from the organism, that is distinguished with characteristic features from necrosis. Cleavage of the DNA by endogenous endonuclease(s) is the hallmark of apoptosis, and the neighbouring cells rapidly incorporate the apoptotic cells, preventing the release of their content, hereby the induction of inflammation. Chemicals and irradiation can induce apoptosis, as well as crosslinkage of cell surface receptors. The best characterized receptors are the Fas receptor (Apo-1, CD95) and the TNFR1, having similar intracellular sequences, the 'death domain', which is necessary for the transduction of the apoptotic signal. There are intracellular adaptor molecules, associated with the death domain, which act as mediators between the receptors and the ICE-like (interleukin-1β converting enzyme) proteases. Apoptosis have a central role in the maturation and functioning of the immune system. In mice mutations in the gene of the Fas receptor or its ligand result in impaired activation induced cell death, which leads to the development of an autoimmune lymphoproliferative syndrome, resembling systemic lupus erythematosus. Some alterations of apoptosis were also detected in patients with systemic autoimmune diseases as well as in some infectious deseases, such as AIDS and hepatitis. An important function of apoptosis is the elimination of malignant cells. However, genetic damage of some oncogens and tumour suppressor genes (e.g. p53) may lead to impairment regulation of apoptosis and results in the survival of the transformed cells.
|Translated title of the contribution||The role of apoptosis in physiological and pathological processes|
|Number of pages||8|
|Journal||Lege Artis Medicinae|
|Publication status||Published - Jun 4 1998|
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