Apoptosis and Programmed Cell Death in Immunity

Abstract

Death of some cells in the mammalian body is clearly programmed. In the immune system there are many examples of programmed cell death, during development of lymphocytes as well as at later stages, after interaction with antigen. Many of these examples display the morphology of apoptosis: They undergo shrinkage and zeiosis, the nucleus collapses, and chromatin is cleaved into nucleosomal fragments. The cell is rapidly recognized by phagocytes and disposed of without releasing its contents. In some but not all cases of apoptosis, new macromolecular synthesis is required. Cytotoxic T cells induce changes in their targets that are morphologically apoptotic. The mechanism of apoptosis is currently under active investigation.

An ICE‐like protease is a common mediator of apoptosis induced by diverse stimuli in human monocytic THP.1 cells

“…In order to ensure that the biochemical events studied lie on a common pathway, apoptosis was induced by mechanistically diverse stimuli which act within their own private pathways [5]. Our results indicate that in THE1 cells an ICE-like protease is a common mediator of apoptosis induced by diverse stimuli acting by different mechanisms.…”

“…It has been proposed that all cells except blastomeres would die by apoptosis in the absence of survival signals [4]. The ability of cells to undergo apoptosis can be induced by diverse stimuli including chemicals, radiation and viruses [3,5]. These diverse stimuli trigger a range of different signalling events, including elevations in cytosolic Ca 2÷, cAMP accumulation, alterations in protein kinase C and tyrosine kinase activities, oxidative stress, generation ofceramide or nitric oxide [6].…”

“…These diverse stimuli trigger a range of different signalling events, including elevations in cytosolic Ca 2÷, cAMP accumulation, alterations in protein kinase C and tyrosine kinase activities, oxidative stress, generation ofceramide or nitric oxide [6]. These different signals ellicit a common response by apparently converging on a single pathway(s) characterised by common biochemical and morphological changes of apoptosis [3,5].…”

Role of caspases and possible involvement of retinoblastoma protein during TGFβ-mediated apoptosis of human B lymphocytes

“…Our knowledge of the mechanisms of TGFb-induced apoptosis is still poor and results essentially from studies on hepatic cells (Chen and Chang, 1997;Choi et al, 1998;Chuang et al, 1994;Fan et al, 1996;Inayat-Hussain et al, 1997). Apoptosis is an active energy-dependent process which is characterized by morphological changes including loss of cell volume, plasma membrane blebbing and cell shrinkage, expression of phosphatidylserine on the outer lea¯et of the cell membrane, chromatin condensation, DNA fragmentation into oligo-nucleosomesized fragments and nuclear fragmentation (Cohen et al, 1992). There is growing evidence indicating that members of the ICE/CED-3 protease family play key roles in the execution phase of apoptosis (Cohen, 1997;Henkart, 1996;Salvesen and Dixit, 1997).…”

The SV40 T‐antigen induces premature apoptotic mammary gland involution during late pregnancy in transgenic mice

“…The biochemical hallmark of apoptosis is the non-random DNA fragmentation. This oligonucleosomal DNA fragmentation is specific for many forms of apoptosis including mammary gland involution [10][11][12][13]. To demonstrate further that premature cell death accounts for the under-development of the mammary glands at late pregnancy and during the lactation period, the DNA was extracted from normal and transgenic mammary glands and subjected to agarose gel electrophoresis.…”