✍ Scribed by J. Malejczyk; A. Górski
No coin nor oath required. For personal study only.
Apoptosis or programmed cell death (PCD) plays a part in a wtriety of physiological and pathological phenomena. 1'2 It is also actively involved in regulation of the immune response. Current studies on the role of PCD in immunity are focused mainly on elucidation of the mechanisms leading to activation and execution of cell death as well as on its significance for homeostasis of the immune system. These topics were discussed during the International Symposium on Apoptosis and its Role in Immunity held on October 20, 1996 in Warsaw, Poland.
The mechanism of PCD induction depends on the nature of the pro-apoptotic signal. Factors capable of inducing and/or modulating PCD include a variety of physical (ionizing radiation, UV light), chemical (drugs, toxins) and biological (hormones, cytokines, infection, antigens) fiactors. 2 Some of these factors act via specific receptors and induction of PCD involves activation of specific signal transduction pathways.
It appears that different mechanisms of PCD induction lead to a common executing system. The best candidates for central PCD executors are the members of the interteukin-l[3 converting enzyme (ICE)/Ced3 family of cysteine proteases) '4 As presented by Douglas R. Green (La Jolla Institute of Allergy and Immunology, La Jolla, USA), these enzymes are able to induce direct apoptotic changes in isolated nuclei. Possible nuclear targets for ICE/Ced3 proteases include poly-ADP ribose polymerase (PARP), small ribonucleoproteins, topoisomerases and nuclear lamins. Cytosolic substrates may include the elements of the cytoskeleton. Activation of these proteases appears to be crucial for induction of various forms of PCD and their specific inhibition provides protection against cell death.
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